G     000  005  485     8 


vIvXwXw 


THE  LIBRARY 

OF 

THE  UNIVERSITY 

OF  CALIFORNIA 

LOS  ANGELES 

GIFT  OF 


SAN  FRANCISCO 
COUNTY  MEDICAL  SOCIETY 


DISEASES    OF    THE    HEART 


Diseases  of  the  Heart 


THORACIC    AORTA. 


BYROM  BRAMWELL.  M.D.,  F.R.C.P.E., 

LECTURER    ON     THE    PRINCIPLES    AND     PRACTICE    OF    MEDICINE,     AND    ON    PRACTICAL    MEDICINE    AND 
MEDICAL   DIAGNOSIS   IN    THE    EXTRA- ACADEMICAL   SCHOOL   OF  MEDICINE,    EDINBURGH  ;    PATHO- 
LOGIST TO  THE    EDINBURGH  ROYAL    INFIRMARY;    ADDITIONAL   EXAMINER    IN  CLINICAL 
MEDICINE     IN     THE     UNIVERSITY     OF     EDINBURGH.  LATE      PHYSICIAN     AND 

PATHOLOGIST   TO    THE    NEWCASTLE-ON-TYNE    INFIRMARY  ;     FORMERLY 
MEDICAL   OFFICER    TO   THE  TYNEMOUTH    UNION   WORKHOUSE 
HOSPITAL,    THE    PRUDHOE   MEMORIAL   CONVALESCENT 
HOME,     THE     TYNE      FLOATING     HOSPITAL, 
ETC.,    ETC. 


"WITH     317     ILXjTJSTI2,.A^TIOIsrS. 


NEW    YORK  : 
D.    APPLETON    &    CO.,    BOND    STREET. 

1884. 


[.-///  Rights  Resened.\ 


Library 


tioo 
3737^ 


Cn  fHentoriam. 

T.  B.  v.. 


624142 


PREFACE. 

In  the  following  pages,  which  are  based  on  portions  of  my 
Lectures  on  the  Principles  and  Practice  of  Medicine,  and  on 
Practical  Medicine  and  Medical  Diagnosis,  I  have  endeavoured 
to  give  a  systematic  account  of  the  Diseases  of  the  Heart  and 
Thoracic  Aorta.^ 

My  attention  was  early  directed  to  the  diseases  of  the 
heart,  for  soon  after  entering  practice  I  met  with  a  long 
series  of  rare  and  interesting  cardiac  cases.  During  the  past 
fifteen  years  I  have  been  constantly  thinking  and  talking 
about  the  subject,  and  steadily  accumulating  the  clinical 
knowledge  and  pathological  material  necessary  for  the  pro- 
duction of  such  a  work. 

The  lithographs  of  naked-eye  objects,  represent  with  few 
exceptions  the  hearts  of  patients  who  have  been  under  my 
own  care  during  life,  and  with  whose  clinical  histories  I  am 
intimately  acquainted.  The  microscopical  lithographs  are,  with 
two  exceptions,  copied  from  sections  made  by  myself  In 
order  to  ensure  absolute  accuracy  of  representation,  the  naked- 
eye  specimens  were  first  photographed  and  then  drawn  under 
my  immediate  personal  supervision,  while  the  microscopical 
objects  have  been  placed  directly  on  the  stone  from  my  own 
drawings. 

'  The  subject  niattei'  of  the  work  was  delivered  ahnost  exactly  as  it  stands,  in 
the  form  of  lectures  to  the  author's  class  at  the  beginning  of  the  winter  session 
1883-84. 


viii  Preface. 

I  am  particularh^  indebted  to  Professor  Turner  for  his 
kindness  and  libcralit}'  in  allowing  me  to  photograph  and 
reproduce  the  rare  and  beautiful  specimens  which  are  shown 
in  figs.  1 70',  171,  242,  243,  244,  262,  and  281,  and  which  are 
contained  in  the  Anatomical  Museum  of  the  University  of 
Edinburgh.  I  am  also  indebted  to  Professor  Greenfield  and 
Dr  \V}'llic,  with  whose  kind  consent  two  specimens  (figs  169 
and  263)  which  came  under  m\-  notice  in  the  course  of  my 
work  as  Pathologist  to  the  Edinburgh  Royal  Infirmary, 
are  represented. 

My  thanks  are  also  due  to  Professor  Pettigrew,  Drs 
Walshe,  Sansom,  Galabin,  Eothergill,  Green,  Macalister, 
Dudgeon,  and  The  Executors  of  the  late  Dr  Peacock,  for 
their  kindness  in  allowing  me  to  reproduce  some  of  the 
figures  which  have  appeared  in  their  respective  works  ;  and 
to  Messrs  J.  and  A.  Churchill,  Messrs  Longmans,  Green  and 
Co.,  and  Messrs  Macmillan  and  Co.,  for  permitting  me  to 
cop}',  or  to  have  electrotypes  of  cuts,  from  works  which  they 
publish. 

I  must  also  express  my  indebtedness  to  the  numerous 
writers  whose  opinions  are  referred  to  in  the  text,  and  more 
especiall}-  to  Drs  Walshe,  Sibson,  Sansom,  and  Galabin. 

B.  B. 


23  Drumsheugh  Gardens. 
Edinburgh,  .ATay  1884. 


CONTENTS. 


CHAPTER    I. 

PACK 

INTRODUCTORY  ANATOMICAL  AND  PHYSIOLOGICAL  RE- 
MARKS—THE ARTERIAL  BLOOD  SUPPLY  OF  THE  HEART  —  THE 
AUTOMATIC  MECHANISM  OF  THE  HEART  —  THE  NERVOUS 
SUPPLY  OF  THE  HEART  —  THE  CONNECTIONS  OF  THE  SYMPA- 
THETIC WITH  THE  HEART —  THE  CONNECTIONS  OF  THE 
PNEUMOGASTRIC  WITH  THE  HEART —  THE  MANNER  IN  WHICH 
THE  VAGUS  AND  SYMPATHETIC  NERVES  AFFECT  THE  HEART — 
THE  RELATIONSHIP  BETWEEN  THE  HEART  AND  THE  MINUTE 
BLOOD  VESSELS.  .  .  .  .  .  .  .  I-45 

CHAPTER    II. 

THE  GENERAL  PATHOLOGY  OF  THE  HEART.       .  .  .      46-56 

CHAPTER    III. 

THE  CLINICAL  INVESTIGATION  OF  CASES  OF  CARDIAC 
DISEASE — METHOD  OF  CASE-TAKING — SUMMARY  OF  SYMPTOMS — 
THE  PHYSICAL  EXAMINATION  OF  THE  HEART — INSPECTION  — 
PALPATION — PERCUSSION — AUSCULTATION — THE  PHYSICAL  EX- 
AMINATION OF  THE  AORTA  AND  GREAT  BLOOD  VESSELS — THE 
EXAMINATION  OF  THE  PERIPHERAL  ARTERIES — THE  SPHVGMO- 
GRAPH — THE  EXAMINATION  OF  THE  VENOUS  SYSTEM.  .    57-295 


Contents. 


CHAPTER   IV. 

PACE 

DISEASES  OF  THE  PERICARDIUM— ACUTE  PERICARDITIS— 
PERICARDIAL  ADHESIONS—  INDURATIVE  -  MEDIASTINO-PERI- 
CARDITIS  —  CHRONIC  PERICARDITIS  —  HVDROPES  ICARDIUM  — 
PNEUMOPERICARDIUM — H^MOPERICARDIUM.         .  .  296-359 


CHAPTER   V. 

DISEASES  OF  THE  ENDOCARDIUM  —  ACUTE  SIMPLE  EN- 
DOCARDITIS—  ULCERATIVE  ENDOCARDITIS  — CHRONIC  ENDO- 
CARDITIS—  CHRONIC  VALVULAR  LESIONS  —  MITRAL  INCOM- 
PETENCE— MITRAL  STENOSIS— AORTIC  INCOMPETENCE — AORTIC 
STENOSIS— TRICUSPID  INCOMPETENCE— TRICUSPID  STENOSIS  — 
PULMONARY  STENOSIS— PULMONARY  INCOMPETENCE.       .  360-559 


CHAPTER  VI. 

DISEASES  OF  THE  MYOCARDIUM  — ACUTE  MYOCARDITIS — 
CHRONIC  MYOCARDITIS  OR  FIBROID  DEGENERATION— PARTIAL 
ANEURISMS  OF  THE  HEART— HYPERTROPHY  AND  DILATATION — 
HYPERTROPHY  OF  THE  LEFT  VENTRICLE— HYPERTROPHY  OF 
THE  RIGHT  VENTRICLE— HYPERTROPHY  OF  THE  AURICLES 
— ATROPHY  OF  THE  HEART — FATTY  INFILTRATION  —  FATTY 
DEGENERATION— SPONTANEOUS  RUPTURE — NEW  GROWTHS  IN 
THE    HEART.   .......  560-658 


CHAPTER  VII. 

THE    CARDIAC    NEUROSES  —  PALPITATION  —  INTERMITTENT 
ACTION— ANGINA  PECTORIS.  ....  659-689 


Contents.  xi 


CHAPTER   VIII. 

PAGE 

DISEASES  OF  THE  THORACIC  AORTA — ACUTE  AORTITIS  — 
ATHEROMA  —  GENERAL  DILATATION  —  ANEURISMS  — COARCTA- 
TION  OF   THE   AORTIC   ARCH.  ....  690-749 


APPENDIX. 

THE  CARDIOGRAPH.  .....  l^^'lll 


INDEX.    ...  775 


CORRIGENDA. 

Page  56,  three  lines  from  the  bottom,  instead  of  'g//fl;ged'  read  'gff//ged.' 

Page  10,  instead  of  '  Sedg^wick  '  read  '  Sedgwick.' 

Fig.  281,  first  line  of  description,  instead  of  'a  bridge  of  muscular  tissue  (b) 
being  left  between  them,'  read  'a  bridge  of  muscular  tissue  being  left  between 
them.' 


LIST  OF  ILLUSTRATIOxNS. 


FIG. 

1  Heart  of  Dugong, 

2  Bifid  Apex  in  Human  Heart, 

3  Course  of  the  Circulation, 

4  Muscular  Fibres  of  Heart, 

5  Do.,  Do., 

6  Diagram  of  Reflex  Theory  of  Cardiac  Contraction,    . 

7  and  8  Nerves  and  Ganglia  on  Surface  of  Calf's  Heart, 
9  Diagrammatic  representation  of  the  Coronary  Plexuses, 


10  Do.,  Do.,  the  Cardiac  Plexus,  . 

1 1  Semi-diagrammatic  representation  of  the  Connections 

of  the  Sympathetic  with  the  Heart, 

12  Semi-diagrammatic  representation  of  the  Connections 

of  the  Pneumogastric  with  the  Heart,    . 

13  Semi-diagrammatic    representation    of    the    Nervous 

Supply  of  the  Heart  as  a  whole, 

14  The  Last  Cervical  and  First  Thoracic  Ganglia  of  the 

Rabbit,  ..... 

15  Diagram   of   Reflex    Theory  of   Contraction    of   the 

Blood  vessels,    ..... 

16  Diagram  of  Cheyne-Stokes' Respiration, 

17  to  22    Diagrams    illustrative    of   the    Mechanism   of 

Cheyne-Stokes'  Respiration, 

23  Position  of  the  Heart  and  Great  Vessels, 

24  Regions  on  the  front  of  the  Chest,     .  .         Alodi 

25  Area  of  Pulsation  in  a  case  of  Congenital   Displace- 

ment of  the  Heart,         .... 

26  Displacement  of  the  Heart  by  left  Pleuritic  Effusion, 

27  Do.,  Do.,  in  Cirrhosis  of  the  Lung, 

28  Do.,  Do.,  the  result  of  Ascites, 

29  Do.,  Do.,  by  an  enlarged  Liver, 

30  Do.,  Do.,  the  result  of  Emphysema, 

31  Outline  of  Hypertrophied  Left  Ventricle, 

32  Outline  of  Hypertrophied  Right  Ventricle,    . 

33  Relationship  of  the  Heart  to  the  Lungs, 

34  Area  of  Prsecordial  dulness  in  middle  age,     . 

35  Relationship  of  the  Heart  to  the  surrounding  Viscera, 


Owen, 
Original, 
Modified  from  Dalton, 

QUAIN, 

Schweigger-Seidel, 
Original, 
Pettigrew, 
Original, 
Do., 


I-AGK 
2 


Do. 


Do. 


Do. 


Foster, 


2 

4 
8 

9 
13 
17 
18 
17 

23 

24 
26 


Original, 

42 

? 

60 

Original, 

76 

SlBSON, 

94 

Hed  from  Walshe, 

96 

Original, 

106 

SiBSON,  modified. 

108 

Do., 

109 

Do., 

III 

Do., 

112 

Do., 

1 12 

Von  Dusch, 

114 

Do., 

"5 

SiBSON, 

123 

Weil, 

124 

Do., 

126 

XIV 


List  of  Illustrations. 


36  Diagrammatic  Representation  of  the  Cardiac  Cycle,  Original, 

37  Do.,  Do.,  Do.,    Gairdner  &  Sharpey, 

38  Diagram  of  the  Position  of  the  Cardiac  Valves,       JModificd from  Gee, 

39  Diagrammatic  Representation  of  the  Cardiac  Cycle,  Original, 

40  Diagram  illustrative  of  Pseudo-reduplication  of  the 

Pleart  Sounds,  .....  Sansom, 

41  to  48  Diagrammatic  representation  of  Cardiac  Murmurs,    Original,    173 
49  to  54  Diagrams  illustrative  of  the  direction  of  Pro- 
pagation of  Cardiac  Murmurs,    .  .  .  Do.,        182 

55  Sphygmogram  in  Aortic  Stenosis,     .  .  Do., 

56  Do.,        in  Mitral  Stenosis,     .  .  .  Do., 

57  and  58  Diagrams  of  the  Effects  of  IMitral  Lesions 

on  the  Circulation,         ....  Do.,       217, 

59  Diagram  of  the  Effects  of  Aortic  Lesions  on  the  Cir- 
culation, .....  Do., 

60,  61,  and  62  IMahomed's  modification  of  Marey's 
Sphygmograph, 

63  and  64  Dudgeon's  Sphygmograph,    . 

65  Marey's  Sphygmograph  applied  to  the  Wrist, 

66  to  76  Sphygmograms  in  Health  and  Disease, 

77  Dudgeon's  Sphygmograph  applied  to  the  Wrist, 

78  to  124  .Sphygmograms  in  Health  and  Disease, 

125  Mahomed's  method  of  gauging  High  Tension, 

126  to  138  Sphygmograms  in  Disease,     . 
139  and  140  Tracings  of  Jugular  Pulsation, 
141   to  144    Naked    Eye    appearances  of   the    heart    in 

Pericarditis,       .... 

145  Section  through  the  Healthy  Pericardium,    . 

146  to  157  Microscopical  Sections  from  Pericarditis  and 

Pericardial  Adhesions,  . 

158  Pericardium  distended  with  fifteen  ounces  of  fluid, 

159  Distention  of  the  Pericardium  with  2)%  lbs.  of  fluid, 

160  Outline  of  the   Percussion   Dulness  in    Pericardial 

Effusion,  .....  Do., 

161,  162,  and  163  The  Pulsus  Paradoxus. 

KussMAUL,  Ziemssen,  and  Traube,  350, 
164  and  165  Early  Endocarditis, 

166  Vegetations  on  the  Mitral  Valve, 

167  Section  through  the  Normal  Endocardium,  . 

168  Ulcerative  Endocarditis  of  the  Aortic  Valve, 

169  Do.  Do.  Aortic  and    Mitral, 
with  Rupture  of  Chorda-  Tendinere 

170  and  170'  Aneurisms  on  JNIitral  Valve, 

171  Ulceration  of  the  anterior  segment  of  the  Mitral  A'alve, 

173  Ball-like  masses  of  Micrococci, 

174  Section  through  the  aortic  valve  in  Endocarditis, 
174'  Colonies  of  Micrococci,        .... 


I'AGE 

137 
138 
140 
158 

165 
-179 

•186 

213 

217 

218 


Do., 

236 

Dudgeon 

, 

238 

Do., 

240 

Original, 

242-245 

Dudgeon 

, 

246 

Original, 

248 

-277 

Mahomed, 

278 

Original, 

281 

-286 

'"riedreich, 

292 

Original, 

300 

QUAIN, 

303 

Original, 

304 

-306 

SiBSON, 

320 

Do., 

320 

321 


Traube,  350 

351 

Green, 

365 

Original 

366 

QUAIN 

367 

Onginal 

402 

Do. 

Do. 

Do. 

403 

Osler, 

404 

Original, 

404 

Osler, 

404 

List  of  Illustrations. 


XV 


Original, 

405 

ZlEGLER, 

405 

Original, 

416 

Do., 

417 

QUAIN, 

422 

SiBSON, 

422 

VTacalister 

,     423 

Do., 

423 

Original, 

424 

Do., 

Do., 

425 

Do., 

436 

Do., 

442 

Do., 

445 

175  Section  through  the  Mitral  Valve  in  Endocarditis,  . 
175'  Section  through  a  Cardiac  Vegetation, 

176  Chronic  Endo-myocarditis,  .... 
176'  Chronic  Endocarditis,  .... 

177  Aortic  and  Mitral  Valve  Segments,  . 

178  Aortic  and  Mitral  Orifices  in  the  Calf's  Heart, 

179  Base  of  the  Ventricles  in  Systole, 

180  Cross  section  of  the  Ventricles  in  Systole,    . 

181  Aortic  and  Mitral  Valve  Segments,  . 

182  Section  through  the  Left  Auricle  of  a  Child, 

183  Do.,  Do., 

184  Effects  of  a  Mitral  Lesion  on  the  Venous  Circulation, 

185  Direction  of  propagation  of  Mitral  Systolic  Murmurs, 
186,  187,  and  188  Sphygmograms  in  Mitral  Regurgitation, 
189,  190,  and  191  Cardiograms  in  Mitral  Regurgitation,  Sansom  &  Galabin,  448 
192  Pulse  Tracing  in  Pernicious  Anasmia,  .  .  Oi-igiiial,  453 
'93)   ^94)   195'   196)   197)  and  198  Naked  Eye  appear- 
ances of  the  Heart  in  Mitral  Stenosis,  .             .        .         Do.,  478 

199  Direction  of  propagation  of  the  Presystolic  Murmur,  Do.,  485 

200  Diagram  of  Diastolic  Mitral  Murmurs,  .  .  Do. ,  486 

201  Diagram  of  Cardiac  Murmur  and  Sounds  in  Mitral 

Stenosis,  .....  Do.,  488 

202,  203,  204,  and  205  Cardiograms  in  Mitral  Stenosis,  Galabin  &  .Sansom,  489 

206  Pulse  Tracing  in  Mitral  Stenosis, 

207  Aortic  Valve  Flaps,  ..... 

208  Ulceration  of  Aortic  Valve  Flaps,     . 

209  Atheroma  and  Disease  of  Aortic  Valve  Flaps, 

210  Aortic   Regurgitation   and    Dilatation   of  the   Left 

Ventricle,  ..... 

211  Direction  of  propagation  of  Aortic  Diastolic  Murmurs, 

212  and  213  Sphygmograms  in  Aortic  Regurgitation, 
214  and  215  Cardiograms  in  Aortic  Regurgitation, 

216  Direction  of  propagation  of  Aortic  Systolic  Murmurs, 

217  and  218  Sphygmograms  in  Aortic  Stenosis, . 
219  and  220  Pulse  Tracings  in  Pernicious  Anaemia, 

221  Direction  of  propagation  of  Tricuspid  Systolic  Murmur, 

222  to  228  Constriction  of  the  Pulmonary  Orifice, 


Original, 

492 

QUAIN, 

499 

Original, 

502 

Do., 

502 

Do., 

503 

Do., 

512 

Do., 

514 

Galabin, 

515 

Original, 

525 

Do., 

526 

Do., 

529 

Do., 

536 

229  Course  of  the  Circulation  in  the  Fcetus, 

230  Direction   of    propagation   of    Pulmonary   Systolic 

Murmur,  ..... 

231,  231,'  232,  and  233  Muscular  Fibres  in  Myocarditis, 
233   and    234    Sections    through    the    Left   Ventricle    in 

Chronic  Mitral  Disease, 

235  Atrophy  of  the  Papillary  Muscles,     . 

236  Endo-peri-myocarditis, 

237  Subacute  Myocarditis, 
238,  239,  240,  and  241   Chronic  Myocarditis, 


Peacock,  544,  545 
Modified  from  QuAlx,   546 


Original, 

550 

Do., 

562 

Do., 

563 

Do., 

568 

Do., 

568 

Do., 

568 

Do., 

569 

XVI 


List  of  Illiistraiions. 


242  Aneurism  of  the  Left  Ventricle, 

243  and  244  Aneurism  of  the  Septum  Ventriculorum,     . 

245  Section  through  a  commencing  Cardiac  Aneurism,  . 

246  Outline  of  Hypertrophied  Left  Ventricle,     . 

247  and  248  Cardiograms  in  Hypertrophy  of  the  Left 

\'entricle,  .  .  . 

249,  250,  and  251  Sphygmograms  in  Hypertrophy  of 
the  Left  Ventricle,        .... 

252  Hypertrophy  of  the  Right  Ventricle, 

253  Cardiogram  in  Hypertrophy  of  the  Left  Auricle, 

254  Cardiogram  in  Dilatation  of  the  Left  Ventricle, 

255  and  256  Atrophy  of  the  Heart, 

257  Fatty  Infiltration  of  the  Heart, 

258  Fatty  Degeneration  of  the  Heart,     . 

259  and  260  Spontaneous  Rupture  of  the  Heart, 
261  and  262  Tumours  of  the  Heart, 

263  Blood-cyst  in  the  Heart, 

264  Section  of  Aorta,  in  Atheroma, 

265  Do.,  Do., 

266  Sphygmogram  in  Atheroma, 

267  Saccular  Aneurism  of  the  Abdominal  Aorta, 

268  and  269  Aneurisms  of  the  Thoracic  and  Abdominal 

Aorta,    ...... 

270  Aneurism  of  the  Sinuses  of  Valsalva, 

271  and  272  Section  through  the  wall  of  an  Aortic  Aneurism, 
273  and  274  Obliterative  Endarteritis,     . 

275,  276,  277,  and  278  Sphygmograms  in  Aneurisms, 

279  and  280  Sphygmograms  in  Aneurism, 

281   Rupture  of  an  Aortic  Aneurism  into  the  Left  Auricle, 

282,  283,  284,  285,  and  286  Aneurism  of  the  commence- 
ment of  the  Thoracic  Aorta, 

287  and  288  Aneurism  of  the  transverse  portion  of  the 
Aortic  Arch,      ..... 

289  Aneurism  rupturing  into  the  Q£sophagus,     . 

290  Erosion  of  the  Spine  by  the  pressure  of  an  Aneurism, 
291,  292,  293,  and  294  Clots  from  the  interior  of  Aneurisms, 
295  and  296  Sphygmograms  from  a  case  of  Aneurism,    . 
297  and  298  Coarctation  of  the  Thoracic  Aorta, 

299  Galabin's  Cardiograph,         .... 

300  Marey's  Tambour,     ..... 

301  Normal  Cardiographic  Tracing, 

302  Normal  Cardiographic  Wave, 

303  Heart  Curve  from  the  Ventricle  of  a  Cat, 


Original, 

576 

Do., 

576 

Do., 

577 

Von  Dusch, 

564 

G A LAB IN, 

595 

Original, 

596 

Von  Dusch, 

601 

Galabin, 

602 

Do., 

622 

Original, 

630 

Do., 

635 

Do., 

641 

Do., 

653 

Do., 

654 

Do., 

656 

Do., 

692 

Do., 

693 

Do., 

696 

Do., 

698 

Do., 

Do, 

Do.. 

Do., 

Do., 

715 

Do., 

716 

Do.. 

720 

Do.. 

Do., 

Do.. 

Do., 

Do., 

Do., 

Walshe, 

Galabin, 

Marey, 

Galabin, 

Eiilayged from  Galabin, 

Foster, 


721 


304  Simultaneous    Tracings,    from    the    interior    of   the 

Right  Auricle  and  Right  Ventricle,  and  of  the 

Cardiac  Impulse  in  the  Horse,  .  .         Ch.\uve.\u  &  Marey, 

305  to  317  Cardiographic  Tracings  in  disease      .         Galabin  &  Sansom, 


735 
747 
754 
756 
759 
760 
761 


762 
763 


DISEASES  OF  THE  HEART. 


CHAPTER    I. 

INTRODUCTORY  ANATOMICAL  AND  PHYSIOLOGICAL  REMARKS  THE 
ARTERIAL  BLOOD-SUPPLY  OF  THE  HEART.  THE  AUTOMATIC 
MECHANISM  OF  THE  HEART.  THE  NERVOUS  SUPPLY  OF  THE 
HEART.  THE  CONNECTIONS  OF  THE  SYMPATHETIC  WITH  THE 
HEART.  THE  CONNECTIONS  OF  THE  PNEUMOGASTRIC  WITH  THE 
HEART.  THE  MANNER  IN  WHICH  THE  VAGUS  AND  SYMPATHETIC 
NERVES  AFFECT  THE  HEART.-  THE  RELATIONSHIP  BETWEEN 
THE  HEART  AND  THE  MINUTE  BLOOD-VESSELS 

The  consideration  of  the  Diseases  of  the  Circulatory  System 
is  a  subject  of  great  importance,  for  it  embraces  many 
affections  which  are  of  every  day  occurrence  in  practice, 
which  entail  a  vast  amount  of  suffering,  and  which  are  very 
frequently  the  cause  of  death. 

The  diseases  of  the  Circulatory  System  include^ — 

1.  The  diseases  of  the  Heart  and  Pericardium. 

2.  The  diseases  of  the  Arteries. 

3.  The  diseases  of  the  Veins. 

In  treating  of  the  Diseases  of  the  Heart  and  Pericardium, 
I  shall  first  describe  the  methods  of  clinical  examination 
which  are  in  common  use  for  investigating  the  condition  of 
these  structures,  directing  attention,  as  I  proceed,  to  those 

'  The  diseases  of  the  Lymphatics  are  sometimes  included  under  this  head,  but 
they  are,  I  think,  more  appropriately  considered  under  the  disorders  of  the 
Chylopoietic  \'iscera. 

A 


2  Diseases  of  the  Heart. 

points  in  their  anatomy,  physiology,  and  pathology,  which 
are  essential  for  the  due  comprehension  of  our  subject. 
After  the  reader  has  become  thoroughly  familiar  with  these 
points,  I  shall  consider  the  individual  affections  of  the  heart 
and  pericardium  in  detail. 

TRELIMINARY  ANATOMICAL   AND  PHYSIOLOGICAL 
CONSIDERATIONS. 

The  heart— the  central  organ  of  the  circulation— may  be 
regarded  as  a  muscular  pump  ;  or,  speaking  more  accurately, 
it  may  be  said  to  consist  of  two^  muscular  pumps, — the 
systemic  and  pulmonary  hearts  respectively. 

Each  half  or  pump  consists  of  two  chambers,  viz.,  (i)  a 
receiving  chamber  or  auricle,  and  (2)  a  propelling  chamber  or 
ventricle. 

'  At  an  early  period  of  fcEtal  life,  as  in  the  permanent  state  of  the  Dugong 

*  (see  fig.  l),  the  heart  is  so  deeply  cleft  from  the  apex  towards  the  base,  as  almost 

to  give  the  idea  of  two  separate  ox^TiXi's..— Carpenter'' s  Physiology,  p.  271.     In  the 

adult  heart  of  man,  the  remains  of  the  deep  cleft  are  sometimes  seen  in  the  form 

of  a  bifid  apex  (see  fig.  2). 


Fig.  I. — Heart  of  Dugong  seen  anteriorly:  shows  bifid  apex,  s,  right  auricle. 
q,  right  ventricle,  t,  left  auricle,  r,  left  ventricle,  u,  aorta  giving  off  innominates, 
left  carotid  and  left  subclavian  arteries,  v,  pulmonary  artery  bifurcating  and  pro- 
ceeding to  right  and  left  lungs. — {After  Owen.) 

Fig.  2.  Apex  of  the  human  heart  (half  the  natural  size)  showing  a  deep  cleft, 
A,  between  the  two  ventricles. 


Prcliiuinary   Considerations.  3 

The  function  of  the  auricle  is  to  receive  the  blood  which  is 
carried  to  it  by  the  great  veins,  to  store  up  that  blood  for  a 
brief  period  {i.e.  the  period  corresponding  to  the  ventricular 
systole),  and  to  transmit  it  to  the  ventricle.  The  function  of 
the  ventricle  is  to  propel  the  blood,  which  it  receives  from 
the  auricle,  into  the  great  artery  which  arises  from  it,  and 
thence  through  the  arterial  system  and  round  the  vascular 
circle.^ 

The  backward  flow  of  blood  from  the  ventricle  to  the 
auricle  is  partly  prevented  by  the  auriculo-ventricular  valve 
segments,  partly,  as  Ludwig,  Hesse,  and  Macalister  have 
shown,  by  the  contraction  of  the  muscular  wall  of  the 
ventricle  itself,  i.e.  by  the  contraction  of  the  muscular  fibres 
which  surround  the  valvular  orifice.  The  backward  flow 
from  the  arterial  system  (aorta  or  pulmonary  artery)  into 
the  ventricle,  is  prevented  by  certain  valvular  arrangements, 
which  I  shall  afterwards  describe  in  detail  ;  while  the 
backward  flow  of  blood  from  the  auricles  to  the  veins 
is  partly  prevented  by  the  contraction  of  the  muscular 
fibres,  which  are  placed  at  their  points  of  termination,  i.e. 
where  the  veins  join  the  heart,  the  systemic  venous  circula- 
tion being  still  further  protected  from  the  '  backwash,'  which 
not  unfrequently  occurs  through  the  tricuspid,  even  in  con- 
ditions of  health,  by  the  valves  of  the  veins  themselves.  By 
these  means  the  onward  flow  of  blood  in  one — a  forward — 
direction  is  accurately  maintained. 

The  course  of  the  circulation  is  diagrammatically 
represented  in  figure  3,  while  '  the  passage  of  the 
blood  through  the  heart  takes  place  in  the  following 
manner : — - 

At  the  commencement  ot  the  auricular  diastole  (and 
while  the  ventricular  systole  is  taking  place)  blood  begins 
to    flow   from   the    great  venous    trunks    into    the    auricular 

'  The  chief  cause,  ol  the  motion  of  the  blood,  is  the  heart,  but  the  onward 
passage  of  blood  is  also  aided  by  the  contraction  of  the  blood  vessels.  This 
contraction  is  partly  the  result  of  elasticity,  and  partly  due  to  an  active  contraction 
of  the  muscular  coat. 


Diseases  of  the  Heart. 


KIG.     3. 


Course  of  the  Circulation.  5 

Description  o/FlG.  3. — Diagraiiintatic  representation  of  the  course  of  t lie  circulation. 
^Modified  from  Dal  ton. ) 

The  arrows  indicate  the  course  of  the  circulation. 

RV,  the  right,  and  LV,  the  left  ventricles. 

RA,  the  right,  and  LA,  the  left  auricles. 

Lungs,  Liver  (description  in  full). 

S,  Stomach. 

Spl,  Spleen. 

In,  Intestines. 

K,  Kidneys. 

Sc,  Supra-renal  capsules. 

P,  Pelvic  viscera. 

LE,  Lower  extremities. 

UE,   Upper  extremities  and  superficial  parts  of  the  head  and  neck. 

B,  Brain. 

Sp,  Spinal  cord. 

PA,  Pulmonary  artery. 

PV,  Pulmonary  veins. 

AA,  Branches  of  the  ascending  aorta. 

DA,  Descending  aorta. 

SV,   Superior  cava. 

IV,  Inferior  cava. 

1  Cccliac  axis,  sending  branches  to  the  spleen,  stomach,  and  liver. 

2  Mesenteric  arteries. 

3  Renal  arteries. 

4  Arteries  to  the  pelvic  viscera. 

5  Arteries  to  the  lower  extremities. 

6  Arteries  to  brain  and  spinal  cord. 

7  Arteries  to  brain. 

8  Arteries  to  spinal  cord. 

9  Arteries  to  the  upper  extremities  and  superficial  parts  of  the  head  and  neck. 

10  Hepatic  veins. 

1 1  Portal  vein. 

12  Veins  from  the  intestine  (superior  and  inferior  mesenteric  veins). 

13  Veins  from  the  stomach  and  spleen. 

14  Splenic  vein. 

15  Coronary  and  pyloric  veins  from  the  stomach. 

16  Renal  veins. 

17  Veins  from  the  pelvic  viscera. 

18  Veins  of  the  lower  extremities. 

19  Veins  from  the  brain  and  spinal  cord. 

20  Veins  from  the  brain. 

21  Veins  from  the  spinal  cord. 

22  Veins  from  the  upper  extremities  and  superficial  parts  of  the  head  and  neck. 


6  Diseases  of  tJie  Heart. 

cavities ;  as  soon  as  the  ventricular  diastole  occurs  the  ven- 
tricles dilate,  the  pressure  in  the  ventricular  cavities  becomes 
negative,  and  blood  flows  from  the  auricles  into  the  ven- 
tricles through  the  auriculo-ventricular  (mitral  and  tricuspid) 
orifices  ;  before  long  the  auricles  become  full  of  blood,  and 
the  auricular  systole  occurs ;  the  muscular  contraction  com- 
mences in  the  walls  of  the  great  veins,  and  spreads  in  a 
peristaltic  manner  over  the  auricles,  which  sharply  contract 
and  discharge  their  blood  into  the  ventricles,  distending 
them,  and  bringing  the  segments  of  the  auriculo-ventricular 
valves  into  close  apposition  ;  the  muscular  contraction  now 
passes  to  the  ventricles,  the  auriculo-ventricular  orifices  are 
firmly  closed  by  the  muscular  contraction,  to  which  I  have 
alread}'  referred,  the  valve  segments  are  tensely  stretched, 
the  arterial  valves  are  burst  open,  and  the  ventricles  empty 
themselves  into  the  aorta  and  pulmonary  artery ;  the  great 
arteries  become  distended,  the  segments  of  the  aortic  and 
pulmonary  valves  are  floated  together ;  the  recoil  of  the 
aorta  and  pulmonary  artery  then  occurs,  and  the  aortic  and 
pulmonary  valves  are  closed  and  stretched. 

Now  in  studying  both  the  physiology  and  pathology  of 
the  heart,  and  in  investigating  its  diseases  at  the  bedside, 
it  is  essential  to  keep  this  fact  constantly  in  view,  that  the 
heart  is  not  merely  a  mechanical,  but  that  it  is  also  a  muscular 
pump,  and  that,  as  Professor  Michael  Foster  so  lucidly  points 
out,  its  action  consequently  presents  problems  which  are 
partly  mechanical  and  partly  vital}  I  cannot  insist  too 
strongly  upon  the  importance  of  looking  at  the  heart 
both  as  a  mechanical  pump  and  as  a  vital  organ  ;  it  is  in 
fact  the  base  upon  which  an  intelligent  comprehension  of 
the  physiology  and  pathology  of  the  heart,  and  of  the 
symptomatology,  diagnosis  and  treatment  of  its  diseases, 
must  be  founded. 

But  although  the  heart  is  a  muscular  organ,  it  differs 
from  the  other  muscles  of  the  body  in  several  important 
particulars.     They  are  as  follows  : — 

'  A  Text  Book  of  Physiology,  p.  IJ5. 


Peculiarities  of  the   Cardiac  Aliiscle.  7 

In  \}aq  first  place,  although  the  cardiac  muscle  is  involun- 
tary in  its  action,  it  is  transversely  striated  in  its  structure — 
a  fact  which,  as  Gaskell  has  pointed  out,  explains  many  of 
the  peculiarities  of  the  cardiac  muscle. 

Dr  Gaskell  looks  upon  the  heart  as  a  specially  modified  portion  of  the 
vascular  system  ;  'the  heart  is  to  be  considered,'  he  says,  'as  a  piece  of 
artery  or  vein,  the  muscular  walls  of  which  have  developed  in  a  special 
manner.  The  keynote  therefore  of  the  peculiarities  of  the  cardiac  muscle 
consists  in  its  structural  position,  intermediate  between  unstriped  and 
striated  muscle  fibre.  Muscular  tissues  exhibit  three  different  modes  of 
responding  to  stimulation  according  to  their  structure.  These  modes 
may  be  expressed  by  saying  that  certain  muscles  possess  essentially  the 
power  of  "tonic  contraction,"  others  the  power  of  "rhythmical  contrac- 
tion," and  others  that  of  "  rapid  contraction."  A  comparison  of  the 
tetanising  action  of  a  strong  interrupted  current  upon  a  strip  of  muscle 
from  the  bladder  of  the  tortoise  and  from  the  heart  of  the  tortoise  with 
the  ordinary  tetanus  curve  of  the  frog's  gastrocnemius  shows  clearly  the 
difference  of  the  three  kinds  of  muscular  tissue. 

'  The  unstriped  muscle  of  the  bladder  contracts  slowly  after  a  long 
latent  period,  the  contraction  increasing  steadily  in  force  during  and  even 
after  the  cessation  of  the  tetanizing  current,  and  then  the  strip  returns 
with  excessive  slowness  to  its  original  length.  In  other  words,  we  see  a 
prolonged  tonic  contraction  as  the  result  of  the  stimulation. 

'With  the  striated  muscle  we  have  the  well  known  curve  of  tetanus 
composed  of  the  superposition  of  a  series  of  rapid  contractions. 

'  The  cardiac  strip  gives  a  curve  which  is  intermediate  between  the 
two,  and  may  be  described  as  consisting  of  a  long  continued  tonic  con- 
traction upon  which  a  number  of  rapid  contractions  are  superimposed. 
These  separate  rapid  contractions  never  succeed  one  another  so  quickly 
as  to  fuse  together.  The  cardiac  muscle  then,  when  tetanized,  gives,  in 
virtue  of  its  relationship  to  unstriped  muscle,  a  tetanus  of  tonicity  (to  use 
Ranvier's  expression),  and  at  the  same  time  a  series  of  rapid  contractions 
in  consequence  of  its  affinity  to  ordinaiy  striated  muscle.  When  the 
vitality  of  the  tissue  is  impaired  by  exhaustion,  by  injurj^,  by  malnutrition, 
the  cardiac  muscle  loses  its  power  of  rapid  contraction,  and  the  less- 
specialized  tonic  power  alone  remains,  the  inuscle  strip  tetanized  when 
in  that  condition  contracts  with  a  prolonged  tonic  contraction  in  the 
same  way  as  unstriped  muscle. 

'  In  another  respect  too,  the  intermediate  position  of  the  cardiac  muscle 
between  the  slowly  contracting,  slowly  exhausted  unstriped  muscle,  and 
the  rapidly  contracting,  easily  exhausted  striated  muscle,  is  clearly 
shown  ;  the  vitality  of  unstriped  muscle  after  the  death  of  an  animal  is 
wonderfully  long  ;  the  irritability  of  the  cardiac  muscle  after  death  is 


Diseases  of  the  Heart. 

that  of  the  ordinarj'  striated 


less  than  this,  but  decidedly  greater  than 
muscles.'^ 


Secondly,  The  structure  of  its  fibres  is  somewhat  different 
from  the  structure  of  the  voluntary  muscles. 

{a)  The  fibres  of  the  heart  are  made  up  of  quadrangular 
portions  (see  fig.  4),  each  of  which  contains  a  nucleus,  and 
each  of  which  may,  therefore,  be  regarded  as  a  distinct  muscle 
cell. 


Fig.   4.  —  Six  muscular  fibre-cells  from  the  heart,  magnified  a,i^  diameters. 
(After  E.A.S.,  Quaiii's  Anatomy,  Ninth  Edition']. 

a,  line  of  junction  between  two  cells;  b,c,  branching  of  cells.  (From  a  drawing 
by  Mr  J.  E.  Neale.) 

iU)  They  have  no  sarcolemma. 

.{c)  They  are  longitudinally  as  well  as  transversel\- 
striated,  and,  in  good  sections,  are  seen  to  be  composed  of 
a  number  of  minute  rods  or  fibres  running  parallel  to  each 
other. 

{d^  They  freely  anastomose,  the  connections  being  formed 


'    The  Journal  of  rhysioloi;y,  vol.  iv.,  No.  2,  p.  II 6. 


Peculiarities  of  the  Cardiac  Muscle.  g 

by  branches  given  off  here  and  there,  from  the  muscle  cells 
of  which  the  fibres  are  composed.     (See  fig.  5.) 


Fig.  5. — Muiciila)-  fibres  from  tlie  heart,  magnified,  showing  their  cross  stria, 
divisions,  and  junctions.  {After  Schweigger-Seidel,  from  Quains  Anatomy, 
Ninth  Edition.  \ 

The  nuclei  and  cell-junctions  are  only  represented  on  the  right-hand  side  of 
the  figure. 

{e)  They  seem  to  be  difiercntly  affected  by  electricity,  the 
Faradic  current,  according  to  Zicmssen's  observations,  being 
much  less  efficacious  in  producing  contractions  and  alterations 
in  rhythm  than  the  galvanic. 

Thirdly,  its  action  is  constant,  and  its  contractions  rhyth- 
mical and  automatic. 


Amongst  the  vital  problems  connected  with  the  heart, 
some  of  the  most  prominent  and  important  are  : — 

(i)  The  manner  in  which  it  receives  its  arterial  blood 
supply. 

(2)  The  construction  and  mode  of  action  of  the  mechanism, 
by   which   its   contractions   are   produced    and    regulated    (its 


lo  Diseases  of  the  Heart. 

automatic  muscular  and  motor  nerve  arrangements),  the 
scnsorium  is  informed  of  its  condition  (its  scjisory  nerve 
arrangements),  the  nutritive  condition  of  its  muscular  fibre  is 
maintained  and  regulated  (its  trophic  nerve  supply). 

(3)  The  construction  and  nature  of  the  nerve  arrange- 
ments, by  means  of  which  it  is  brought  into  relationship  with 
the  other  parts  of  the  vascular  system,  and  with  the  other 
organs  of  the  body. 


The  A  rterial  Blood-supply  of  the  Heart. 

As  we  all  know,  arterial  blood  is  conveyed  to  the  car- 
diac muscle  by  the  coronary  arteries ;  and  until  quite  recently 
it  was  supposed  by  many  of  our  leading  physiologists  and 
physicians,  that  in  consequence  of  the  relative  positions  of 
the  parts,  the  orifices  of  the  coronary  arteries  must  of  neces- 
sity be  closed  during  the  systole  of  the  ventricle — the  valve 
flaps  being  pressed  against  the  orifices  of  the  coronary 
arteries  by  the  blood-stream  in  its  passage  from  the  ven- 
tricle into  the  aorta.  The  recent  experiments,  however,  of 
Martin  and  Sedgwick,  seem  conclusively  to  show  that  this 
supposed  closure  does  not  occur,  and  that  the  coronary,  like 
all  the  other  arteries  of  the  body,  are  distended  during  the 
systole  of  the  heart.  These  observers  have  shown,  by  means 
of  careful  cardiographic  tracings,  that  the  blood-waves  in 
the  coronary  arteries  and  carotids  are  exactly  synchronous 
both  in  normal  and  diseased  states  of  the  circulation.  It 
seems  certain,  therefore,  as  Dr  George  Balfour  and  others 
had  previously  argued,  that  the  blood  is  propelled  into  the 
coronary  arteries  during  the  systole  of  the  heart. 

TJie  Automatic  McchaiiisDi  of  the  Heart. 

The  nervous  mechanism  of  the  heart  is  extremely  com- 
plicated, and  the  manner  in  which  it  acts  is  far  from 
being  perfectly  understood.  It  is  a  subject,  however,  of  the 
greatest  importance,  and  we  must,  therefore,  consider  it  in 
some  detail. 


Mechanisiu  of  tJic  Hearf  s  Beat.  1 1 

In  the  Jijsi place,  it  is  necessary  to  remember  that  the  con- 
traction of  the  heart  is  automatic,  i.e.  it  is  due  to  impulses 
arising  within  the  heart  itself,  and  that,  in  conditions  of 
health,  the  action  of  the  two  sides  of  the  heart,  i.e.  of  the  two 
pumps,  is  synchronous.  Under  ordinary  circumstances  the 
heart  beats  in  a  perfectly  rhythmical  and  regular  manner,  the 
number  of  contractions  being,  in  the  adult  male,  about  72 
per  minute. 

Until  recently  it  was  supposed  that  the  rhythmical 
action  of  the  heart  was  entirely  due  to  the  periodical  and 
orderly  discharge  of  motor  nerve  force  in  the  nerve  ganglia, 
which  are  scattered  through  the  organ,  but  recent  obser- 
vations, more  especially  of  some  German  physiologists  and 
the  brilliant  researches  of  Gaskell,  seem  to  show  that  the 
influence  of  the  cardiac  ganglia  is  not  indispensable,  and 
that  the  muscular  fibre  itself,  in  some  of  the  lower  animals 
at  all  events,  possesses  the  power  of  rhythmical  contraction. 
Gaskell's  observations  seem  to  prove  conclusively,  that,  in 
the  tortoise,  the  automatic  action  of  the  heart  does  not 
depend  upon  any  special  rhythmical  nervous  apparatus,  but 
that  it  is  due  to  a  property  of  rhythmical  contraction  inherent 
in  the  muscular  tissue  itself. 

It  is  perhaps  premature  to  conclude  that  the  automatic 
contractions  of  the  human  heart  are  produced  in  exactly  the 
same  manner  as  the  automatic  contractions  of  the  heart  of 
the  tortoise.  We  may,  however,  safely  say,  that  in  man,  the 
rhythmical  action  of  the  heart  must  be  due,  either  to  the 
periodical  and  orderly  discharge  of  motor  nerve  force  from 
the  ganglia  which  it  contains,  or  to  a  rhythmical  property 
possessed  by  the  muscular  tissue  independently  of  any  special 
nervous  mechanism  ;  and  if  we  may  judge  by  analogy,  the 
latter  view  is  possibly  the  correct  one.  And  this  we  may 
term  the  first  step  in  the  comprehension  of  the  mechanism  of 
these  complicated  arrangements. 

In  the  second  place,  it  would  appear  that  the  stimulus  to 
muscular  contraction  is  the  presence  of  blood,  or  rather  the 
presence  of  blood   under  a   certain   pressure,  in  the   cardiac 


12  Diseases  of  the  Heart. 

cavities.^  If  the  pressure  is  too  low  the  stimulus  is  insuffi- 
cient, and  the  muscle  does  not  contract.  If,  on  the  other 
hand,  the  pressure  is  too  great,  over-distention  and  a  para- 
lytic condition  may  result.  Indeed  the  recently  published 
experiments  of  Sewall  and  Donaldson  seem  to  prove  '  that, 
within  its  working  limits  of  internal  pressure,  the  heart  muscle 
has  a  remarkable  power  of  accommodating  the  intensity  of 
its  discharges  of  energy,  to  the  resistance  to  be  overcome.'  ^ 

'A  fact  continually  forced  upon  our  attention,'  say  these  writers,  '  was 
the  great  dependence  of  the  systole,  as  to  its  energy  and  completeness, 
upon  the  amount  of  fluid  within  the  heart.  Particularly  was  this  noticed 
in  regard  to  the  thin  walled  sinus  and  auricles,  when  isolated  in  the  man- 
ner to  be  described.  Within  tolerably  low  fluid  pressures,  the  sinus 
and  auricles  become  so  distended  as  to  be  powerless  to  contract  ;  as 
the  pressure  within  them  is  reduced  they  contract  feebly,  and  when  the 
quantity  of  blood  flowing  into  them  is  only  just  sufficient  to  bring  about 
full  distension  during  diastole,  they  contract  powerfully,  and  empty  them- 
selves completely  at  each  beat.  As  the  supply  of  blood  is  further  lessened 
by  lowering  the  pressure  flask,  the  contractions  apparently  again  become 
feebler,  and  in  the  sinus  hardly  visible.'  ^ 

The  exact  manner  in  which  the  cardiac  muscle  is  stimulated  by  the 
presence  of  blood  under  a  certain  pressure  is  obscure.  If  the  muscular 
contraction  can  occur  independently  of  the  ganglia,  we  must  suppose 
either  that  the  muscular  fibre  is  dir-ectly  stimulated  by  the  mechanical 
stretching  which  it  undergoes  when  the  cardiac  cavities  become  dis- 
tended ;  or,  that  the  contraction  is  indirect,  and  is  due  to  stimulation 
of  the  fine  nerve  fibres'*  which,  as  Schweigger-Seidel ^  has  shown,  form 
a  rich  plexus  in  the  endocardium.  If  we  grant  that  the  ganglia  are 
concerned  in  the  process,  we  may  suppose,  as  some  physiologists  have 
for  long  held,  that  the  mechanism  is  a  reflex  one.  A  cardiac  ganglion- 
cell  may  be  regarded  as  the  centre  of  a  reflex  arc,  to  which  a  sensory 
nerve  fibre  passes  from  the  endocardium,  and  from  which  a  motor  nerve 

'  In  some  of  the  lower  animals,  the  frog  for  instance,  the  heart  continues  to 
beat  even  after  the  cavities  have  been  cleared  of  blood,  and  indeed  when  they 
are  almost  empty  of  fluid.  In  the  frog,  therefore,  the  presence  of  blood  is  not 
absolutely  necessary  to  produce  cardiac  contractions,  but  it  is  nevertheless  probable 
that  the  pressure  of  the  blood  in  the  cardiac  cavities,  under  ordinary  circumstances, 
acts  as  a  stimulus,  and  excites  the  contraction  of  the  cardiac  muscular  fibres. 

-   The  Journal  of  Physiology,  vol.  iii.  p.  361. 

'  Loc.  cit.  p.  361. 

*■  This  view  necessarily  supposes  that  these  fine  nerve  fibres  are  motor. 

'  Quoted  by  Power,  Carpenter'' s  Physiology,  p.  276. 


Automatic  Mechanism  of  the  Heart.  13 

fibre  proceeds  to  the  cardiac  muscle  (see  fig.  6)  ;  the  reflex  mechanism 
being  thrown  into  action  by  the  presence  of  blood,  under  a  certain 
pressure,  in  the  cavities  of  the  organ. 


Fig.   6. — Diagrammatic  refresentation  of  the  reflex  mechanism  by  which  [it  has 

been   theorised)  the  cardiac  imticle  is  thrown   into  contraction,   under  the 

influence  of  the  blood  pressure. 

E',E,  the  endocardium  ;  B,  the  blood  in  the  cardiac  cavity ;  M,  the  muscular 

fibre  of  the  heart  ;  G,   ganglion  cell,  the  reflex  centre  ;  n,   sensory  nerve  fibre 

conducting  the  impression  generated  by  the  blood  pressure  on  the  sensory  nerve 

terminations  under  the  endocardium  to  the  reflex  centre  ;  n',  motor  nerve  fibril 

conducting  the  impulse  from  the  reflex  centre  to  the  muscle. 

In  the  third  place.,  the  experiments  of  Gaskell,  and  of  Sewall 
and  Donaldson,  seem  to  show  that  in  the  frog  and  tortoise 
at  least,  and  when  the  heart  is  acting  normally,  the  motor  im- 
pulse originates  in  the  sinus,  and  passes  from  the  sinus  to  the 
muscular  fibres  of  the  auricle,  and  thence  to  the  ventricle,  the 
rhythm  of  the  sinus  determining  that  of  the  whole  heart. 

Those  authorities  who  believe  that  the  automatic  action 
of  the  heart  is  due  to  the  periodical  discharge  of  its  motor 
ganglia,  necessarily  conclude,  in  order  to  explain  these  results, 
that  the  action  of  the  ganglia,  which  are  situated  in  the  sinus 
venosus,  is  more  powerful  than  that  of  the  ganglia  situated  in 
other  parts  of  the  organ ;  and  indeed  some  authorities  have  sup- 
posed that  the  ganglia  of  the  sinus  venosus  are  the  true  auto- 
matic centres,  while  the  action  of  the  other  ganglia  requires  to 
be  excited  reflexly,  or  in  some  other  manner.  The  supporters 
of  the  neurotic  theory  further  believe  that  the  sequence  of  the 
cardiac    contractions   (the   fact    that    the    contraction    of  the 


14  Diseases  of  the  Heart. 

auricle  follows  at  a  regular  interval  upon  the  contraction  of  the 
sinus,  and  the  contraction  of  the  ventricle  at  a  regular  interval 
upon  that  of  the  auricle)  is  due  to  nervous  influences. 

Dr  Gaskell,  whose  experiments  seem  to  show,  as  I  have 
already  mentioned,  that  the  automatic  rhythm  originates 
in  the  muscular  tissue  itself,  explains  the  fact  that  the 
contractions  originate  in  the  sinus,  by  the  peculiar  structure 
of  the  cardiac  muscle  in  this  part  of  the  heart ;  while  he  states 
that  the  sequence  of  the  contraction  of  the  ventricle  to  the 
auricle  is  not  due  to  separate  stimuli  passing  along  nerve 
fibres  from  the  sinus  to  the  ventricle — not,  in  short,  to  any 
nervous  mechanism— but  to  the  fact  that  a  wave  of  con- 
traction passes  directly  from  the  muscular  fibres  of  the 
auricle  to  the  muscular  fibres  of  the  ventricle,  through 
the  muscular  fibres  forming  the  auriculo-ventricular  groove. 
The  pause,  or,  more  correctly,  the  alteration  of  rate  in  the 
progress  of  the  contraction  wave,  which  takes  place  between 
the  contraction  of  the  auricle  and  the  contraction  of  the 
ventricle,  is,  he  says,  due  to  an  alteration  in  the  conducting 
power,  which  naturally  exists  at  the  auriculo-ventricular  ring. 
'  This  diminished  conducting  power  or  natural  block,  exists 
not  only  because  the  auriculo-ventricular  muscular  ring  is 
narrow,  and  that  a  somewhat  abrupt  change  occurs  in  the 
direction  of  the  muscular  fibres  along  which  the  contraction 
wave  passes  when  it  reaches  and  leaves  this  ring,  but  essen- 
tially because  the  structure  of  the  muscular  fibres  here  is 
different  from  those  of  the  auricle  or  ventricle. 

'  The  muscle  fibres  throughout  the  heart  ^  are,'  he  states, 
'  of  the  same  type,  any  differences  which  are  seen  are  differ- 
ences in  the  prominence  of  the  various  structural  peculi- 
arities of  the  cardiac  type  of  muscle,  and  are  not  so  great  as 
the  differences  between  unstriated  and  striated  muscle  fibres. 
Thus  all  the  muscle  fibres  are,  to  a  greater  or  less  extent, 
transversely  striated ;  but  the  prominence  of  this  striation  varies 
considerably.  Similarly  the  thickness  of  the  fibre,  the  extent 
of  parallelism  of  its  edges,  the  size  of  the  nucleus  in  relation 
to   the  size  of  the  fibre,  and  therefore  the  extent  of  crowding 

'   He  is  speaking,  it  must  be  remembered,  of  the  adult  heart  of  the  tortoise. 


A^itoniatic  JMechanisiu   of  tJie  Heart.  15 

of  the  nuclei  in  any  strip,  all  present  differences  in  different 
parts  of  the  heart.  The  greatest  contrast  is  seen  when  the 
muscular  fibres  of  the  ground  layer  in  the  sinus  are  teased 
out  and  compared  with  the  muscle  fibres  of  the  spongy  tissue 
of  the  ventricle.  The  sinus  muscle  fibre  is  thin  and  delicate, 
tapering  somewhat  at  both  ends,  with  a  large  central  oval 
nucleus  which  causes  a  distinct  bulging  of  the  fibre ;  the  sub- 
stance of  the  fibre  shows  a  striation  which  is  decidedly  indis- 
tinct, presenting  often  a  granular  rather  than  a  distinct  banded 
appearance.  On  the  other  hand,  the  ventricular  muscle  fibre 
is  boldly  and  strongly  striated,  it  is  much  thicker  than  that  of 
the  sinus,  its  edges  are  parallel,  and  the  thin  elongated  nucleus 
is  small  in  comparison  to  the  size  of  the  fibre.  The  muscle 
fibres  of  the  reticulated  tissue  of  the  auricle  are  not  so  large 
or  so  coarsely  striated  as  those  of  the  ventricle,  though  larger 
and  much  more  distinctly  striated  than  the  sinus  muscle  fibres. 
Their  edges  also  are  more  parallel  than  in  the  fibres  of  the 
sinus.  The  muscular  ring  forming  the  junction  of  the  auricles 
and  ventricle,  and,  to  a  certain  extent,  the  whole  junction  wall 
joining  the  two  auricles,  are  composed  of  muscle  fibres,  with 
a  structure  intermediate  between  the  sinus  and  the  auricle 
muscles.  The  nuclei  are  large,  conspicuous  on  section  both 
in  size  and  number,  the  striation  is  not  so  well  marked  as  in 
the  bulged  portion  of  the  auricles,  and  the  fibres  are  thin  and 
delicate,  with  somewhat  parallel  edges. 

'  Such  a  structure  as  above  described  is  very  suggestive, 
not  only  as  an  explanation  of  the  pauses  which  occur  natur- 
ally in  the  course  of  the  peristaltic  wave  of  contraction,  but 
also  of  the  differences  of  rhythmical  power  exhibited  by 
different  parts  of  the  heart.' ^ 

Dr  Gaskell,  therefore,  conceives  '  that  the  variations  in  the 
rhythmical  power  and  in  conductivity,  which  are  characteristic 
of  the  different  parts  of  the  adult  heart  of  the  tortoise,  may  all 
be  accounted  for  on  the  supposition,  that  the  development 
of  the  muscular  tissue  of  the  originally  tubular  heart  has 
not  proceeded  at  the  same  rate  throughout  the  tube,  so  that  in 
the  adult  heart   greater  variations  in  rhythmical   power  arc 

'  Journal  of  riiysiology,  vol.  iv.  pp.  72,  73. 


1 6  Diseases  of  tJie  Heart. 

apparent  in  the  different  sections  of  it,  than  in  the  original 
tubular  heart ;  the  peristaltic  wave  of  contraction  which 
originally  passed  smoothly  from  end  to  end,  passes  finally 
along  a  tube  of  irregular  calibre,  the  muscular  walls  of  which 
have  become  so  modified  in  their  rates  of  contraction  and 
conduction,  as  well  as  in  the  arrangement  of  the  fibres,  as  to 
form  out  of  a  simple  peristaltically  contracting  tube  such  an 
efficient  muscular  pump  as  is  represented  by  the  adult  heart.^ 

'  The  conception  advanced  above,  that  the  rhythmical 
beating  of  the  heart  is  due  to  a  series  of  peristaltic  con- 
tractions which  start  from  that  particular  portion  of  the 
muscular  tissue  of  the  heart  in  which  the  property  of  auto- 
matic rhythm  has  been  most  largely  developed,  brings  the 
heart's  action  into  harmony  with  the  rfest  of  the  vascular 
system  and  with  the  rhythmical  properties  which  are  so  often 
manifested  by  the  less  specialized  forms  of  muscular  tissue.'^ 

Space  will  not  allow  me  to  detail  the  facts  and  arguments 
on  which  Dr  Gaskell  founds  this  theory,  which  obviously  has 
most  important  practical  bearings  on  the  pathology  of  the 
human  heart.  I  would,  however,  strongly  advise  my  readers 
to  peruse  the  original  for  themselves. 

In  the  fourth  place,  Gaskell  has  distinctly  proved  that  the 
ventricle  is  supplied  with  afferent  nerve  fibres,  which  are  '  able 
to  regulate  the  force  of  the  auricular  contractions,  as  well  as 
in  all  probability  the  rate  of  rhythm.  It  is  then  conceivable 
that  the  function  of  many  of  the  nerve  fibres  which  pass  into 
the  ventricle  is  by  their  action  upon  the  force  of  the  auricular 
contractions  to  regulate  the  amount  of  blood  thrown  into  the 
\-entriclc,  and  therefore  the  amount  of  work  done  by  the  heart.' ^ 

But  although  the  movements  of  the  heart  are  automatic,  it 
is  intimately  connected  both  with  the  sympathetic  and  cerebro- 
spinal nervous  centres  ;  and  its  action  can,  as  each  one  of  us  so 
well  knows,  be  readily  affected  by  general  nervous  influences. 
But  in  order  that  this  most  important  and  difficult  part  of  our 
subject  may,  if  possible,  be  clearly  understood,  I  must  now 
describe  the  nervous  supply  of  the  heart  in  some  detail. 

'  Journal  of  Physiology,  vol.  iv.  p.  77.     -  Loc.  cit.  p.  80.      ^  Loc.  cit.  p.  92. 


The  Nervous  Supply  of  the  Heart.  i  7 

Delicate  nerve  fibres  are  met  with  in  considerable  numbers 
both  on  the  surface  and  in  the  substance  of  the  heart ;  and 
nodular  enlargements,  which  microscopic  examination  has 
shown  to  be  true  nervous  ganglia,  i.e.  to  contain  nerve  cells, 
are  abundantly  distributed  on  certain  of  these  nerve  fibres, 
and  on  the  numerous  points  of  junction  which  certain  of  the 
fibres  make  with  each  other.  In  the  human  subject  the 
nerves  of  the  heart  are  neither  so  numerous  nor  so  distinct  as 
in  some  of  the  lower  animals,  as,  for  example,  the  calf  (see  figs. 
7  and  8) ;  but  even  in  man  '  the  surface  and  substance  of 
the  heart  are  enveloped  in  a  more  or  less  uniform  plexus.'  (^The 
Physiology  of  the  CircnlatioUy  by  J.  Bell  Pettigrew,  p.  298.) 


FIG.    7.  FIG.   8. 

Fig.  7. — Nerves  and gangliaon  the  anterior  surf  ace  of  the  calf 's  heart.  {After  Pettigrew.) 

a,  b,  pulmonary  artery  and   aorta  with   nerve-plexuses  and  ganglia.      ?',   de- 
scending cava  with  nerve-plexus  and  ganglia,     c,  right  auricle,     d,  left  auricle. 
e.  Nerves  and  ganglia  distributed  on  right  side  of  heart.    /,  ditto  on  left  side. 
g,  anterior  coronary  vessels  covered  with  nerve-plexuses  and  ganglia. 
Fig.  8. — Nervcsandgangliaonthcposteriorsurfaceofthecalfs heart.  {After Pettigrew, ) 

i,  descending  cava,  c,  nerves  and  ganglia  on  right  auricle,  d,  ditto  on  left. 
e,  nerves  and  ganglia  on  right  ventricle,  f  ditto  on  left.  /,  great  nerve-plexus  and 
ganglia  covering  coronary  sinus  (r)  and  extending  itself  on  the  right  (//),  left  (/),  and 
posterior  coronary  vessels,  and  the  right  {e)  and  left  (/)  ventricles  generally.  The 
ganglia  in  this  case  are  very  numerous,  particularly  on  the  coronary  sinus  (r). 

B 


1 8  Diseases  of  the  Heart. 

Both  nerve  fibres  and  nerve  cells  are  most  numerous  and 
most  distinct  in  the  grooves  which  contain  the  larger  branches 
of  the  coronary  arteries,  and  anatomists  have  consequently 
described  a  rigJit  and  a  left  coronary  plexus. 

The  coronary  plexuses  (see  fig.  9)  may  be  said  to  be 
composed  of  branches  proceeding  to  the  heart  from  the 
so-called  cardiac  plexus,  which,  to  a  large  extent  at  least, 
surrounds  the  arch  of  the  aorta. 

The  right  coronary  plexus  (R  C  P)  accompanies  the  branches  of 
the  right  coronary  arter)^,  and  sends  branches  (a,  b)  both  to  the  right 
auricle  and  right  ventricle.  It  receives  branches  (c,  d)  from  both  the 
superficial  (S  C  P)  and  deep  (D  C  P  )  cardiac  plexuses  (see  fig.  10)  the 
composition  of  which  I  shall  presently  describe. 

The  left  coroftary  plexus  (L  C  P),  which  is  larger  than  the  right,  is 
composed  of  two  primaiy  divisions  (represented  as  one  ganglion  cell  in  the 
figure),  corresponding  to  the  primary'-  divisions  of  the  left  coronary  artery. 
The  branches  proceeding  to  it  (e)  are  almost  entirely  derived  from 
the  left  half  of  the  deep  cardiac  plexus  (D'C'P'),  a  few  filaments  only  (f) 
passing  to  it  from  the  right  half  (DPC).  The  branches  proceeding  from 
it  (g,  h,  i)  are  distributed  to  the  left  auricle  and  to  both  ventricles. 


RA 


aY— 


Fig.   9. — Diagrammatic  representation  of  the  coronary  plexuses. 

RCr,  right,  and  LCP,  left  coronary  plexuses;  RV,  right,  and  LV,  left  ventricles 
of  the  heart ;  RA,  right,  and  LA,  left  auricles ;  SVC,  superior  vena  cava, 
a,  branch  of  the  right  coronary  plexus  to  the  right  auricle ;  b,  to  the  right  ven- 
tricle ;  c  and  d,  branches  proceeding  to  the  right  coronary  plexus  from  the  super- 
ficial, and  deep  cardiac  plexuses  respectively  ;  e  and  f,  branches  proceeding  to 
the  left  coronary  plexus  from  the  left  and  right  halves  of  the  deep  cardiac  plexus 
respectively  ;  g,  branch  proceeding  from  the  left  coronary  plexus  to  the  left  auricle  ; 
h,  to  the  left  ventricle  ;  i,  to  the  right  ventricle, 


The  Coronary  Plexus  of  Nerves.  19 

TJie  cardiac  plexus  (see  fig.  jo,  S  C  P,  D  C  P  and  D'C'P') 
may  be  described  as  partly  surrounding  the  arch  of  the  aorta. 
In  it  all  the  cardiac  branches  of  the  sympathetic  and  of  the 
pneumogastric  and  its  branches,  terminate,  and  from  it, 
branches  proceed  to  the  heart.  In  this  great  cardiac  plexus 
the  numerous  nerve  filaments,  proceeding  to  and  from  the 
heart,  are  re-arranged  and  re-distributed,  and  by  this  means 
the  heart  is  brought  into  most  intimate  connection  with 
many  distant  parts  —  a  connection  which  the  practical 
physician  should  always  keep  in  view,  for  it  explains  many 
of  the  symptoms  (apparently  unconnected  with  the  heart) 
which  are  met  with  in  association  with  cardiac  disease. 

The  cardiac  plexus  has  been  artificially  divided  by  an- 
atomists into  two  'parts,  which  are  respectively  termed  the 
superficial  and  deep  cardiac  plexuses. 

The  sifpe?'Jicial  car-diac  plexus  (S  C  P)  lies  for  the  most  part  in 
the  concavity  of  the  aortic  arch.  In  it  the  first,  or  superficial  cardiac 
nerve  of  the  left  side  (I'C'N'),  and  the  lower  cervical  branch  of  the  left 
pneumogastric  (8',  fig.  lo)  terminate  ;  and  from  it  branches  (c)  proceed 
to  the  right  coronary  plexus.  It  also  gives  a  few  small  filaments  (j  and  k) 
to  the  pulmonary  artery  and  anterior  pulmonary  plexus  of  the  left  side. 

The  deep  cardiac  plexus  (D  C  P  and  D'  C  P'),  which  is  considerably 
larger  than  the  superficial,  is  situated  '  behind  the  arch  of  the  aorta, 
between  it  and  the  trachea,  and  above  the  bifurcation  of  the  pulmonary 
arteiy.'i 

In  it,  all  the  branches  of  the  sympathetic  and  pneumogastric  pro- 
ceeding to  the  heart,  except  the  first  or  superficial  cardiac  branch  of  the 
left  sympathetic  and  the  lower  cervical  branch  of  the  left  pneumo-gastric, 
terminate. 

The  deep  cardiac  plexus  is  described  as  consisting  of  two  halves 
(right  and  left). 

The  right  half{T>  C  P)  sends  branches  to — 

(i.)  The  right  coronary  plexus  (d). 

(2.)  The  right  auricle  (1). 

(3.)  The  left  coronary  plexus  (a  few  filaments)  (f). 

The  great  majority  of  the  branches  of  the  Icfi  half  (e)  proceed  to  the 
left   coronary   plexus  ;   a  small    number    (o)    passing   to    the   superficial 

'  Q^tain's  Anatomy,  Ninth  Edition,  vol.  i.  p.  661,  from  which  I  have  largely 
drawn  in  this  description. 


20 


Diseases  of  the  Heart. 


cardiac  plexus.     A  few  filaments  (the  small  branch  above  the  letter  k  in 
fig.  12),  proceed  to  the  anterior  pulmonary  plexus  on  each  side.^ 

V-    ICN 


3CN 


DCP 


RA- 


SV- 


D'C'P' 


Fig.    10. — Diai^raininatic  rcpresentatioii  of  tlic  cardiac  plexus.      The  different 
divisions  of  the  plexus  are  shown  as  ganglion  cells. 

SCP,  superficial  cardiac  plexus  ;  DCP,  right,  and  D'C'P',  left  halves  of  the 
deep  cardiac  plexus  ;  ICN,  first  or  superficial  cardiac  nerve  on  the  right  side  ; 
I'C'N',  first  or  superficial  cardiac  nerve  of  the  left  side,  2CN,  right,  and  2'C'N', 
left  middle  cardiac  nerves;  3CN,  right,  and  3'C'N',  left  lower  cardiac  nerves; 
8',  lower  cervical  branch  of  the  left  ]ineumogastric  proceeding  to  the  superficial 
cardiac  plexus,  9,  9,  branches  of  the  right  pneumogastric  proceeding  to  the  right 
half  of  the  deep  cardiac  plexus  ;  r'c'l'  and  9',  branches  of  the  left  recurrent 
largyngeal  nerve  proceeding  to  the  left  half  of  the  deep  cardiac  plexus  ;  c,  branch 
from  the  superficial  cardiac  plexus  to  the  right  coronary  plexus  ;  j,  k,  branches  to 
the  pulmonary  artery  and  pulmonary  plexus  of  the  left  side,  d  and  f,  branches 
from  the  right  half  of  the  deep  cardiac  plexus  to  the  right  and  left  coronary 
plexuses,  respectively ;  1,  branch  to  the  right  auricle,  e,  branches  from  the  left 
half  of  the  deep  cardiac  plexus  to  the  left  coronary  plexus  ;  o,  branch  to  the  super- 
ficial cardiac  plexus.     The  other  letters  have  the  same  significance  as  in  fig.  II. 


'  According  to  Pettigrew  a  few  of  the  branches  forming  the  superficial  cardiac 
plexus  pass  backwards  and  appear  on  the  posterior  surface  of  the  heart ;  while  a 
certain  number  of  the  branches  of  the  deep  cardiac  plexus  pass  forwards  to  appear 
on  its  anterior  surface  {Physiology  of  the  Circtilntion,  p.  298). 


The  Cardiac  Plexus  of  Nerves. 


21 


The  cardiac  plexus  then  is  a  'junction'  at  which  impulses 
passing  to  and  from  the  heart  may  be  transferred  from  one 
nerve  path  to  another,  and  by  means  of  which  communica- 
tions are  established  between  the  heart  and  distant  parts. 
The  '  main  lines  '  which  pass  between  the  nerve  centres  and 
the  heart  are  the  sympathetic  and  pneumogastric.  In  order 
to  complete  the  anatomical  description  of  the  cardiac  nerves, 
I  must  now  detail  the  origin  and  connections  of  their  cardiac 
branches. 


THE   CONNECTIONS   OF   THE   SYMPATHETIC   WITH   THE 

HEART. 

Each  of  the  three  cervical  ganglia  of  the  sympathetic 
sends  a  branch  to  the  heart,  the  upper,  middle,  and  lower 
eardiae  nerves  respectively  (see  fig.  1 1). 


The  upper  or  siiperjicial  cardiac  nerve  of  the  right  side  (1  C  N)  arises 
by  two  or  more  branches  from  the  upper  cervical  ganglion,  and  some- 
times also  by  a  branch  from  the  trunk  of  the  sympathetic,  which  joins 
the  upper  and  middle  cervical  ganglia.  After  proceeding  down  the  neck 
it  enters  the  thorax,  being  directed  along  the  innominate  artery  to  the 
back  of  the  arch  of  the  aorta,  where  it  terminates  in  the  deep  cardiac 
plexus  (D  C  P).  In  its  course  through  the  neck  and  in  the  thorax,  it 
forms  numerous  connections  with  other  branches  of  the  sympathetic  and 
of  the  pneumogastric,  the  more  important  of  which  are — 

1.  A  connection  with  the  external  laryngeal  branch  of  the  pneumo- 
gastric (l). 

2.  A  connection  with  the  trunk  of  the  pneumogastric  {2). 

3.  A  connection  with  the  recurrent  laryngeal  branch  of  the  pneumo- 
gastric (3). 

It  also  sends  some  small  branches  to  the  thyroid  body,  and  to  the 
front  of  the  great  vessels  (aorta  and  pulmonary  artery). 


The  upper  or  superficial  cardiac  nerve  of  the  left  side  (I'C'N')  arises 
in  the  same  manner,  and  has  the  same  course  through  the  neck  as  its 
fellow  of  the  right  side.  After  entering  the  chest  it  is  directed  along  the 
left  common  carotid  artery  to  the  front  of  the  arch  of  the  aorta,  which  it 
crosses,  and  terminates  in  the  superficial  cardiac  plexus  (S  C  P).  In 
exceptional  cases  this  nerve  terminates  in  the  deep  cardiac  plexus. 


2  2  Diseases  of  the  Heart. 

The  middle^  deep,  or  great  cardiac  Jterve  of  the  right  side  (2  C  N) 
arises  from  the  second  cervical  ganglion  of  the  sympathetic.  After 
entering  the  chest  it  lies  in  front  of  the  trachea,  and  ends  in  the  right  half 
of  the  deep  cardiac  plexus.     It  forms  connections  with — 

1.  The  upper  cardiac  branch  of  the  sympathetic  (4). 

2.  The  recurrent  laryngeal  branch  of  the  pneumogastric  (5). 

The  middle  cardiac  nerve  of  the  left  side  has  the  same  origm,  course, 
and  connections  as  the  corresponding  nerve  on  the  right  side.  It 
terminates  in  the  left  half  of  the  deep  cardiac  plexus. 

The  lower  cardiac  nerve  of  the  tight  side  arises  from  the  third  cervical 
ganglion,  or  from  the  first  dorsal  ganglion  of  the  sympathetic,  enters  the 
thorax  behind  the  subclavian  artery,  and  terminates  in  the  right  side  of 
the  deep  cardiac  plexus.     It  forms  connections  with — 

(i.)  The  middle  cardiac  branch  of  the  sympathetic  (6). 

(2.)  The  recurrent  laryngeal  branch  of  the  pneumogastric  (7). 

The  hnver  cardiac  nerve  of  the  left  side  has  the  same  origin,  course, 
and  connections  as  the  corresponding  nerve  on  the  right  side.  It 
terminates  in  the  left  side  of  the  deep  cardiac  plexus.  This  nerve  often 
joins  the  middle  cardiac  branch  of  the  same  side,  the  common  trunk  thus 
formed,  ends  in  the  left  side  of  the  deep  cardiac  plexus. 


Description  oj  FiG.    II. — Seini-diagraiinnatic  rcprescntatioti  of  the  connections  of 
the  sympatlietic  with  the  heart. 

ICG  and  I'C'G',  upper  cardiac  ganglia  of  the  sympathetic  (right  and  left). 

2CG  and  2'C'G,  middle  ,,  ,,  ., 

3CG  and  3'C'G,  lower  ,,  ,,  ,, 

icn,  2cn,  3cn,  4cn,  5cn,  6cn,  yen,  Sen,  branches  of  the  right,  first,  second, 
third,  fourth,  fifth,  sixth,  seventh,  and  eighth  cervical  nerves,  proceeding  to  the 
sympathetic  ganglia. 

I'c'n',  2'c'n',  3'c'n',  4'c'n',  5'c'n',  6'c'n',  7'c'n',  8'c'n',  branches  of  the  left, 
first,  second,  third,  fourth,  fifth,  sixth,  seventh,  and  eighth  left  cervical  nerves 
proceeding  to  the  sympathetic  ganglia. 

IDG  right,  and  I'D'G',  left  first  dorsal  ganglia  of  the  sympathetic,  idn 
branches  of  the  right,  and  I'd'n'  left  first  dorsal  nerves  proceeding  to  the  first 
dorsal  ganglia  of  the  sympathetic. 

ICN  right,  and  I'C'N'  left,  first  or  superficial  cardiac  nerves. 

2CN  right,  and  2'C'N'  left  middle  cardiac  nerves. 

3CN  right,  and  3'C'N'  left  inferior  cardiac  nerves. 

The  other  letters  have  the  same  significance  as  in  the  previous  figures 
(  9  and  10). 


TJic   Cardiac  Brandies  of  tJic  Sympathetic.  2, 


ICG. 


Icn. 


2cn. 
3cn. 
4cn. 


2CG 


6cn^ 


■ICN 


I'C 


3CG 


Scn- 


ldn> 


IDG 


''H^^ 


^^ 


3CN 


I'C'G' 


VC'Qf 


3'C'G' 
.I'd'n' 

I'D'C 


3'C'N' 


SVC- 


DCP 


RA- 


av- 


D'C'P' 


24  Diseases  of  the  Heart. 

THE   CONNECTIONS   OF   THE   PNEUMOGASTRIC   WITH 
THE   HEART. 

Nerves  destined  for  the  heart  arise  from  the  trunk  of  the 
pneumogastric,  both  in  the  neck  and  in  the  thorax,  and 
cardiac  branches  are  also  given  off  by  several  of  its  branches 
(see  fig.  12).  Anatomists  consequently  describe  cervical 
cardiac,  and  thoracic  cardiac  branches  of  the  pneumogastric. 

The  cervical  cardiac  branches.— \x\  the  upper  part  of  the  neck  several 
small  twigs  (2)  connect  the  pneumogastric  with  the  upper  cardiac  branches 
of  the  sympathetic  ;  while  the  external  laryngeal  branch  of  the  superior 
laryngeal  nerve,  which  is  a  branch  of  the  pneumogastric,  is  also  con- 
nected with  the  upper  cardiac  branch  of  the  sympathetic  (i). 

In  the  lower  part  of  the  neck  a  branch  of  some  size  (8)  arises  from  the 
trunk  of  the  right  pneumogastric,  as  it  is  about  to  enter  the  thorax.  It 
is  directed  along  the  innominate  artery  to  the  back  of  the  aorta,  being 
usually  blended  into  one  of  the  branches  of  the  sympathetic,  and  ter- 
minates in  the  right  side  of  the  deep  cardiac  plexus.  This  branch  some- 
times arises  from  the  recurrent  laryngeal. 

The  corresponding  nerve  of  the  left  side  (8')  crosses  in  front  of  the  arch 
of  the  aorta,  and  terminates  in  the  superficial  cardiac  plexus. 

Both  nerves  (right  and  left)  give  some  small  twigs  to  the  coats  of  the  aorta. 

77/^?  thoracic  cardiac  b}-anches. — On  the  right  side  several  cardiac 
branches  (9  and  9)  arise  from  the  trunk  of  the  pneumogastric,  and  from  the 
recurrent  laryngeal,  and  pass  to  the  right  side  of  the  deep  cardiac  plexus. 

The  corresponding  branches  from  the  left  side  (9')  usually  come  entirely 
from  the  recurrent  (Quain),  and  pass  to  the  left  side  of  the  deep  cardiac  plexus. 

In  fig.   13   I  have  endeavoured   to  represent   the   nervous 
mechanism  of  the  heart  in  all  its  complicated  details. 


Description  of  Fig.  12. — Semi-diagrammatic  representation  of  tlie  connections 
of  tlie  pneumogastric  with  tJie  lieai-t. 

PI',  right  pneumogastric  ;  P'P',  left  pneumogastric  ;  rcl,  rcl,  right  recurrent 
laryngeal  nerve  ;  r'c'l',  r'c'l',  left  recurrent  laryngeal  nerve  ;  si,  s'l',  right  and 
left,  superior  laryngeal  nerves  ;  el  and  e'l',  right  and  left,  external  laryngeal  nerves. 
I  and  I',  communicating  branches  between  the  external  laryngeal  nerves  and  the 
first  cardiac  nerves,  on  the  right  and  left  sides  respectively  ;  2  and  2',  between  the 
trunk  of  the  vagus  and  the  first  cardiac  nerve  on  the  right  and  left  sides  respect- 
ively ;  8,  communicating  branch  between  the  trunk  of  the  right  pneumogastric 
and  the  lower  cardiac  nerve  ;  8',  on  the  right  side  this  branch  usually  proceeds 
directly  to  the  superficial  cardiac  plexus  ;  9,  9,  branches  from  the  right  vagus,  in 
the  thorax,  to  the  right  half  of  the  deep  cardiac  plexus  ;  9',  branches  from  the  left 
recurrent  laryngeal  to  the  left  half  of  the  deep  cardiac  plexus. 


The   Cardiac  Branches  of  the   Vagus.  25 


p' 


rcl 


DCP- 


RA- 


D'CT' 


26 


Diseases  of  the  Heart. 


I'C'C 


3CG 


IDG 


DCP 


D'C'P' 


The  Nervous  Supply  of  the  Heart.  27 

Description  jf  Yli;.   13. — Semi-diagrammatic  representation  0/  the  nervous  supply 

of  the  heart. 

RCP,  right,  and  LCP,  left  coronary  plexuses ;  SCP,  superficial  cardiac 
plexuses;  DCP,  right,  and  D'C'P',  left  half  of  the  deep  cardiac  plexus;  P 
right,  and  P'  left  pneumogastric  nerves;  ICG,  Right,  and  I'C'G',  left  superior 
ganglia  of  the  sympathetic  ;  2CG,  right,  and  2'C'G',  left  middle  ganglia  of 
the  sympathetic  ;  3CG,  right,  and  3'C'G',  left  inferior  ganglia  of  the  sympa- 
thetic ;  RV,  right,  and  LV,  left  ventricles ;  RA,  right,  and  LA,  left  auricles ; 
SVC,  superior  vena  cava. 

rcn,  2cn,  3cn,  4cn,  5cn,  6cn,  7cn,  8cn,  branches  of  the  right,  first,  second, 
third,  fourth,  fifth,  sixth,  seventh,  and  eighth  cervical  nerves,  proceeding  to  the 
sympathetic  ganglia. 

I'c'n',  2'c'n',  3'c'n',  4'c'n',  5'c'n',  6'c'n',  7'c'n',  8'c'n',  branches  of  the  left, 
first,  second,  third,  fourth,  fifth,  sixth,  seventh,  and  eighth  left  cervical  nerves 
proceeding  to  the  sympathetic  ganglia. 

IDG  right,  and  I'D'G'  left  first  dorsal  ganglia  of  the  sympathetic,  idn 
branches  of  the  right,  and  I'd'n'  left  first  dorsal  nerves  proceeding  to  the  first 
dorsal  ganglia  of  the  sympathetic. 

si  right,  and  s'l'  left  superior  laryngeal  branches  of  the  pneumogastric ; 
EL  right  and  E'L'  left  external  laryngeal  nerves ;  rcl  right,  and  r'c'l'  left 
recurrent  laryngeal  nerves  at  lower  part  of  neck,  and  in  the  thorax  respectively. 

a,  branch  from  right  coronary  plexus  to  right  auricle ;  b,  branch  from  right 
coronary  plexus  to  right  ventricle ;  c,  branch  from  the  superficial  cardiac  plexus  to 
the  right  coronary  plexus  ;  d,  branch  from  the  right  half  of  the  deep  cardiac  plexus 
to  the  right  coronary  plexus  ;  e,  branch  from  the  left  half  of  the  deep  cardiac 
plexus  to  the  left  coronary  plexus  ;  f,  branch  from  the  right  half  of  the  deep  cardiac 
plexus  to  the  left  coronary  plexus  ;  g,  branch  from  the  left  coronary  plexus  to  the 
left  auricle  ;  h,  branch  from  the  left  coronary  plexus  to  the  left  ventricle  ;  i,  branch 
from  the  left  coronary  plexus  to  the  right  ventricle. 

ICN  right,  and  I'C'N'  left,  first  or  superficial  cardiac  nerves. 

2CN  right,  and  2'C'N'  left  middle  cardiac  nerves. 

3CN  right,  and  3'C'N'  left  inferior  cardiac  nerves. 

I,  branch  from  the  right,  and  l',  branch  from  the  left  external  laryngeal  nerves 
to  the  superior  cardiac  nerves  ;  2,  branch  from  the  right,  and  2',  from  the  left 
pneumogastric  nerves  to  the  superior  cardiac  nerves  ;  3,  communicating  branch 
from  the  right,  and  3',  from  the  left  recurrent  laryngeal  nerves  to  the  first  cardiac 
nerves  on  the  right  and  left  sides  respectively  ;  4,  communicating  branch  between 
the  right,  and  4',  communicating  branch  between  the  left  superior  and  middle 
cardiac  nerves ;  5,  communicating  branch  between  the  right,  and  5'  between  the 
left  middle  cardiac  and  recurrent  laryngeal  nerves  respectively  ;  6,  communicating 
branch  between  the  right,  and  6',  communicating  branch  between  the  left,  middle 
and  inferior  cardiac  nerves  ;  7,  communicating  branch  between  the  right,  and  7', 
between  the  left  inferior  cardiac  nerves  and  the  recurrent  laryngeal  respectively  ; 
8,  communicating  branch  between  the  right  inferior  cardiac  nerves  and  the  trunk 
of  the  pneumogastric,  8',  on  the  left  side  this  branch  of  the  pneumogastric 
proceeds  directly  to  the  superficial  cardiac  plexus  ;  9,  9,  branches  from  the  trunk  of 
the  right  pneumogastric,  and  9',  from  the  left  recurrent  laryngeal  nerve  to  the 
right  and  left  halves  respectively  of  the  deep  cardiac  plexus. 


28  Diseases  of  the  Heart. 

THE   MANNER   IN    WHICH   THE   VAGUS   AND   SYMPATHETIC 
NERVES   AFFECT   THE   HEART. 

I  have  now  described  the  construction  of  the  mechanism 
concerned  in  the  innervation  of  the  heart,  and  I  must  next 
point  out  the  manner  in  which  that  mechanism  works. 

We  have  already  seen  that  while  the  movements  of  the 
heart  are  automatic  {i.e.  are  due  to  impulses  arising  within 
the  heart  itself),  they  can  be  profoundly  modified  by  the 
condition  of  distant  parts  ;  and  that  the  impulses  which 
produce  these  modifications  are  conveyed  to  the  heart 
through  certain  branches  of  the  pneumogastric  and  sym- 
pathetic nerves.  Until  recently,  we  might  have  summed 
up  the  effects  of  these  impulses  by  saying,  that  impressions 
passing  to  the  heart  through  the  pneumogastric,  retard,  ivJiile 
impressions  passing  to  the  heart  through  the  sympathetic, 
accelerate  its  movements  (hence  the  terms  'inhibitor'  and 
'accelerator'  of  the  heart  which  are  given  to  the  two  nerves 
respectively) ;  but  recent  observations  seem  to  show  that  the 
action  of  the  vagus  on  the  heart  is  much  more  complicated, 
and  that  it  affects  not  only  the  rhythm,  but  also  the  force  of 
the  cardiac  contractions,  and  that  it  exerts  a  trophic  influence 
upon  the  cardiac  muscle.  It  will  be  necessary,  therefore,  to 
consider  each  of  these  functions  separately. 

The  Inhibitory  Action  of  the  Vagus. 

As  the  result  of  the  laborious  investigations  of  many  able 
observers,  physiologists  have  concluded  : — Firstly,  that  there 
exists  in  the  medulla  oblongata  a  cardio-inhibitory  centre, 
which  is  continually  exerting  a  restraining  influence  upon  the 
heart  ;  and  Secondly,  that  the  action  of  this  cardio-inhibitory 
centre  may  be  intensified,  i.e.,  the  action  of  the  heart  may  be 
still  further  retarded  by  : — 

(a)  Direct  stimulation,  i.e.,  by  certain  changes  in  the 
medulla  itself. 

(b)  Impressions  passing  to  it  from  the  brain. 


The  InJiibitoiy  Action  of  the    Vagus.  29 

(c)  Impressions  passing  to  it  from  peripheral  parts  (reflex 
stimulation).  ^ 

Some  authorities  also  believe  that  the  cardio-inhibitory  centre  may 
itself  be  inhibited,  i.e.  its  restraining  power  taken  off  the  heart,  by  im- 
pressions passing  to  the  medulla  from  other  parts  of  the  central  nervous 
system,  or  from  the  periphery. 

The  most  important  local  changes  which  stimulate  the 
cardio-inhibitory  centre,  appear  to  be  increased  blood-pressure 
within  the  cranium,  and  irritative  lesions  in  the  medulla  or 
in  the  neighbourhood  of  the  vagi  roots,  e.g.  inflammatory 
affections  at  the  base  of  the  brain,  etc. ;  while  reflex  inhibi- 
tion of  the  heart  seems  to  be  chiefly  brought  about  by  impres- 
sions passing  to  the  medulla  from  the  abdominal  viscera.^ 

It  has  also  been  supposed  that  the  action  of  the  heart 
may  be  inhibited  by  impressions  passing  from  the  heart  itself. 
The  experiments  of  Cyon  and  Ludwig,  Rutherford  and  others, 
seem  to  show  that  reflex  inhibition  of  the  heart  can  be  pro- 
duced in  the  rabbit  by  stimulation  of  the  central  cut  end  of 
the  superior  cardiac  nerve,  the  impression  passing  up  to  the 
cardio-inhibitory  centre  in  the  medulla  oblongata,  and  back, 
through  the  vagus  and  its  inferior  cardiac  branch,  to  the  heart. 

The  superior  cardiac  branch  arises  by  two  roots,  one  connected  with 
its  superior  larj'ngeal  branch  crosses  down  the  neck  close  to  the  cervical 
sympathetic,  and  joins  one  or  two  branches  of  the  inferior  cervical 
ganglion  with  which  it  proceeds  to  the  heart.  This  branch  is  a  purely 
sensitive  nerve  ;  and  is  in  fact  the  sensitive  nerve  of  the  heart.      On 

'  Whether  the  action  of  the  cardio-inhibitory  centre  is  automatic  or  not,  is  still 
undecided. 

*  Powerful  stimulation  of  any  afferent  or  sensory  nerve  can  probably  produce 
reflex  inhibition  of  the  heart.  Rutherford  states  that  the  cardio-inhibitory  fibres 
of  the  vagus  may  be  thrown  into  action  by  stimulating:  (i).  The  central  end  of 
the  vaso-inhibitory  or  superior  cardiac  branch  of  the  vagus  (depressor  nerve)  ; 
(2).  The  central  end  of  the  vagus  of  the  opposite  side  ;  (3).  Almost  any  sensory 
nerve,  in  the  case  of  warm-blooded  animals  ;  (4).  The  abdominal  viscera  of  the 
frog;  (S).  The  splanchnic  and  sympathetic. — Lancet,  Dec.  16,  1871,  page  483. 
Michael  Foster  states  that  '  the  regulative  action  of  the  inhibitory  mechanism  is 
brought  into  more  or  less  close  connection  with  all  parts  of  the  body. — A  Text 
Book  of  Physiology,  p.  174. 


30 


Diseases  of  the  Heart. 


cutting  it  across,  and  stimulating  its  inferior  (peripheral)  end  no  effect 
is  produced  ;  while  stimulation  of  its  upper  (central)  end  causes  pain, 
retardation  of  the  heart,  and,  as  I  shall  afterwards  more  particularly 
point  out,  such  a  striking  diminution  of  blood-pressure,  that  the  term 
depressor  nerve  has  been  given  to  it. 

The  inferior  cardiac  branch  leaves  the  vagus  below  the  origin  of  the 
inferior  lar)-ngeal  nerve,  and  proceeds  directly  to  the  heart.  It  is  a 
cardio-inhibitory  nerve,  and  stimulation  of  its  inferior  cut-end  gives  rise 
to  the  same  effects  as  stimulation  of  the  vagus  itself  {i.e.  stimulation  above 
the  origin  of  this  branch),  viz.  (with  weak  currents)  retardation  of  the 
heart  from  prolongation  of  the  diastole,  and  (with  stronger  currents) 
complete  arrest  during  diastole. 

In  the  rabbit  the  vagus  gives  two  branches  to  the  heart,  a  superior 
and  an  inferior  cardiac  branch  (see  fig.  i6). 


Track 


r/7/i.fAor. 


\V 


n.raff. 


Fig.  li,.  — The  last  ceiT>ical  and  first  thoracic  ganglia  in  the  rabbit.  {Left  side). 
(SoHunvhat diagrammatic,  many  of  the  various  branches  being  omitted.)— 
( .After  Foster. ) 

Trach.  Trachea.  Ca.  carotid  arter)'.  sh.  subclavian  artery.  n.  Vog.  the 
vagiis  trunk,  n.  rec.  the  recurrent  laryngeal,  sym.  the  cervical  sympathetic 
nerve  ending  in  the  inferior  cervical  ganglion,  gl.  cerv.  inf  Two  roots  of  the 
ganglion  are  shown,  7 ad.,  the  lower  of  the  two  accompanying  the  vertebral  arter)^ 
A.  vert. ,  being  the  one  generally  possessing  accelerator  properties,    gl.  thor.  pr^ 


The  Inhibitory  Action  of  the    Vagus.  31 

In  the  human  subject,  two  branches  of  the  vagus  seem 
to  correspond  to  the  superior  cardiac  branch  of  the  vagus 
in  the  rabbit ;  while  the  inferior  cardiac  branch  of  the 
vagus  of  the  rabbit  seems  to  be  (mainly  at  all  events) 
represented  in  man  by  the  large  branch  which  leaves  the 
vagus  trunk  at  the  lower  end  of  the  neck  (inferior  cervical 
branch). 

Now  it  has  been  supposed  that  these  two  nerves,  together 
with  the  cardio-inhibitory  centre  in  the  medulla,  constitute  a 
reflex  arc  ;  and  that  stimulation  of  the  peripheral  terminations 
of  the  superior  cardiac  nerve  in  the  heart  may  generate  an  im- 
pulse which,  being  conveyed  to  the  cardio-inhibitory  centre, 
and  being  reflected  back  to  the  heart  along  the  vagus,  may 
retard  the  action  of  the  heart.  Whether  the  superior  cardiac 
nerve  has  any  special  function  of  this  description,  other  than  is 
possessed  by  all  sensitive  nerves,  is  extremely  doubtful ;  and 
it  seems  certain  that  increased  blood-pressure  within  the 
heart,  as  a  whole,  does  not,  as  was  at  one  time  supposed, 
produce  reflex  inhibition  of  the  organ. 

Physiologists  are  not  yet  agreed  as  to  the  exact  manner 
in  which  the  vagus  causes  inhibition  of  the  heart. 

Until  quite  recently  it  was  believed  that  while  weak 
stimulation  of  the  nerve  prolonged  the  diastole,  the  duration 
of  the  ventricular  systole  being,  very  little  affected,  more 
powerful  stimulation  caused  complete  arrest  during  diastole 
(complete  relaxation),  the  next  systole  being  as  it  were 
indefinitely  postponed  ;  and  it  was  generally  supposed  that 


Description  of  fig.  14.  continued. 
the  first  thoracic  ganglion.  Its  two  branches  communicating  with  the  cervical 
ganglion  surround  the  subclavian  artery  forming  the  annulus  of  Vieussens. 
syi?i.  thai:  the  thoracic  sympathetic  chain.  n.  dep.  depressor  nerve,  which, 
though  running  by  the  side  of  the  sympathetic,  is  really  a  branch  of  the  vagus, 
from  which  it  separates  higher  up.  This  is  joined  in  its  course  by  a  branch  from 
the  lower  cervical  ganglion,  there  being  a  small  ganglion  at  their  junction,  from 
which  proceed  nerves  to  form  a  plexus  over  the  arch  of  the  aorta.  It  is  this 
branch  from  the  lower  cervical  ganglion  which  possesses  accelerator  properties — 
hence  the  course  of  the  accelerator  filires  is  indicated  in  the  figure  by  the  arrows. 


32  Diseases  of  the  Heart. 

the  vagus  inhibited  the  contractions  of  the  heart  by  pre- 
venting motor  impulses  being  sent  from  the  automatic 
gangha  to  the  muscle,  i.e.  by  holding  in,  as  it  were,  the 
motor  energy  of  the  ganglia  ;  and  this  would  appear  to  be 
the  view  which  Sewall  and  Donaldson  take.  They  think 
that  their  experiments  'point  pretty  clearly  to  the  con- 
clusion, that  the  inhibitory  action  of  the  vagus  nerve  exerts 
itself  in  the  same  indirect  way  (as  a  motor  stimulus 
does),  influencing  the  ventricle  by  damping  in  sinus  and 
auricles  the  excito-motor  discharges  arising  in  these  parts  of 
the  heart.' ^ 

Dr  Gaskell  takes  a  different  view.  He  has  shown:— 
Firstly,  that  the  vagus  is  able  to  modify  all  the  great 
functional  attributes  of  the  cardiac  muscle,  viz.: — 

{a)  The  rate  at  which  automatic  contractions  are  pro- 
duced.    (The  automatic  rhythm.) 

{b.)  The  force  with  which  the  contractions,  more  especially 
the  contractions  of  the  auricle,  are  carried  out.  (The  fojre  of 
contraction.) 

(c.)  The  facility  with  which  the  contractions  are  conducted 
by  the  muscular  fibres.     (The  poiver  of  conduction'-.) 

Sccondty,  that  it  sometimes  produces  depression,  at  other 
times  exaltation,  of  function. 

He  believes  that  the  vagus  may  produce  standstill  or 
inhibition  of  the  heart  (auricles  and  ventricles)  in  the  three 
following  ways  : — 

(i.)  By  producing  cessation  of  its  automatic  contractions, 
i.e.  by  depressing  the  rhythmical  power  of  the  muscular  fibres 
of  the  sinus  in  which  the  automatic  rhythm  originates.  (This 
has  been  established  in  the  frog,  tortoise,  and  snake.) 

(2.)  By  reducing  the  force  of  the  auricular  contractions,  so 
that  they  become  invisible,  i.e.  by  depressing  the  contraction 
power  of  the  rapidly  contracting  reticulated  muscular  fibres 
of  the  auricle.     (Frog.)     The  contractions,  he  states,  may  be 

'  Joitrnal  of  Physiology,  vol.  iii.  p.  367. 

^  In  the  tortoise  the  force  of  the  contractions  of  the  ventricle  was  uninfluenced 
by  vagus  stimulation.  In  the  frog,  on  the  other  hand,  the  vagus  influences  the 
force  of  the  ventricular  as  well  as  of  the  auricular  contractions. 


The    Trophic  Action  of  the  Vagus.  33 

so  small  as  only  just  to  be  visible,  so  that  to  the   naked  eye 
the  heart  appears  to  stand  still. 

(3.)  By  blocking  the  contraction  wave  at  the  sino-auricular 
ring,  i.e.  by  depressing  the  conducting  power  of  the  muscular 
fibres  connecting  the  sinus  and  auricle.    (Snake,  tortoise,  frog.) 

The  Trophic  Function  of  the  Vagus. 

As  I  have  previously  remarked,  Dr  Gaskell  has  advo- 
cated the  important  theory,  which  Eichorst  had  previously 
advanced,  that  the  vagus  is  the  trophic  nerve  of  the  heart. 
'  Although,'  he  says,  '  the  initial  effect  of  the  vagus  is  to  de- 
press some  function,  its  final  and  most  enduring  power  is  to 
exalt,  intensify,  and  repair  that  function.  Thus,  although 
it  slows  rhythm,  yet  its  stimulation  makes  the  rhythmical 
power  last  longer  than  it  otherwise  would,  and  makes  the 
heart  beat  with  regularity  when  it  was  previously  irregular  ; 
although  it  reduces  the  force  of  the  contractions,  yet  its  ulti- 
mate effect  is  to  improve  and  sustain  the  contraction  force  ; 
although  it  may  diminish  the  conduction  power,  yet  in  the 
end  it  completely  repairs  that  power.  For  these  reasons,'  he 
says,  '  /  took  upon  tlie  vagus  as  essentiatty  tlie  tropliic  nerve  oj 
the  Jicarti^ 

Since  this  chapter  was  written,  I  have  learned  from  Dr 
Gaskell  that  the  term  '  trophic,'  as  it  is  commonly  used  and 
understood,  does  not  exactly  express  the  function  which  he 
supposes  the  vagus  to  have  over  the  cardiac  muscle.  '  I  have 
felt,'  he  says,  '  all  along  that  the  word  trophic  is  somewhat 
misleading  as  applied  to  the  results  of  my  experiments  on 
the  action  of  the  vagus.  I  wanted  a  word  to  express,  what 
appears  to  me  to  be  the  fact,  in  the  cold-blooded  animals  at 
all  events,  that  the  inhibitory  process  is  not  destructive  but 
constructive  in  its  nature,  but  could  not  find  any  good  term. 
I  have  therefore  used  the  word  '  trophic,'  not  perhaps  in  its 
usual  sense,  but  rather  in  a  sense  similar  to  Heidenhain, 
when  he  divides  the  nerves  supplying  the  sub-maxillary 
gland  into  secretory  and  trophic' 


^  Jotirnal  of  Physiology,  vol.  iv.  p.  104, 
C 


34  Diseases  of  the  Heart. 

Tlic  Mode  of  Action  of  t tie  Vagus  on  ttic  Heart. 
The  exact  manner  in  which  the  terminal  fibres  of  the  vagus 
are  brought  into  relation  with  the  cardiac  muscle  is  unknown. 
The  effects  produced  by  vagus  stimulation,  and  by  the  action 
of  certain  poisons,  have  led  some  physiologists  to  believe  that 
the  arrangement  is  an  extremely  complicated  one  ;  and  in 
order  to  explain  these  results,  they  have  theorised  that  there 
existed  an  inhibitory  mechanism  within  the  heart  itself,  the 
action  of  which  is  strengthened  (brought  into  play)  by 
impressions  carried  to  it  by  the  terminal  branches  of  the 
vagus,  and  which  in  its  turn  acts  upon,  i.e.  inhibits  the 
ganglionic  apparatus  more  immediately  concerned  in  the 
production  of  the  rhythmical  movements  of  the  heart,  i.e. 
the  automatic  nerve  mechanism. 

The  facts  and  arguments  which  they  have  advanced  in  support  of  the 
view  that  the  vagus  does  not  act  directly  upon  the  cardiac  muscle,  but 
that  it  acts  through  some  intermediate  nerve  apparatus,  are  as  follows  : — 

1.  The  latent  period,  which  elapses  between  electrical  stimulation  of 
the  vagus  and  the  production  of  its  inhibitory  action  on  the  heart  is 
twenty-times  longer  than  that  which  elapses  between  the  electrical 
stimulation  of  an  ordinary  motor  nerve,  and  the  contraction  of  its  muscle. 
viz.,  3th  and  f^jth  of  a  second  respectively. 

2.  A  very  much  stronger  current  is  required  to  produce  inhibition  of 
the  heart  through  the  vagus,  than  is  required  to  produce  spasm  of  a 
voluntary  muscle,  when  its  motor  nerve  is  stimulated. 

3.  If  the  action  of  the  heart  be  arrested  by  stimulation  of  the 
vagus,  the  rhythmical  contractions  after  a  time  return,  although  the 
stimulation  of  the  vagus  be  continually  kept  up,  a  fact  which  may  be 
explained  either  by  supposing  that  the  inhibitory  fibres  of  the  vagus 
become  gradually  exhausted  by  the  prolonged  stimulation,  or  that  the 
accumulation  of  nerve  force  in  the  automatic  ganglia  becomes  after  a 
time  too  great  to  be  held  back,  and  that  an  explosion  and  muscular 
contraction  consequently  take  place. 

4.  Continued  stimulation  of  one  vagus  annuls  or  prejudices  the  action 
of  the  other. 

5.  '  The  effects  of  vagus  inhibition  are  perhaps  more  marked  when 
the  electrodes  are  placed  on  the  boundary  line  between  the  sinus  venosus 
and  the  auricle,  than  over  the  vagus  trunk  itself.'— iv7j/^r. 

6.  If  during  the  complete  relaxation  which  results  from  powerful 
stnnulation  of  the  vagus,  the  muscular  tissue  be  mechanically  irritated,  it 
is  still  found  to  contract. 


The  TropJiic  Action  of  the  Vagus.  35 

While  the  existence  of  an  intermediate  (intra-cardiac)  inhibitory 
mechanism  between  the  terminal  fibres  of  the  vagus  and  the  automatic 
nerve  apparatus  they  think  proved  by  the  following  circumstances  : — 

1.  When  the  electrodes  are  placed  on  the  boundary  line  between  the 
sinus  venosus  and  the  auricles,  more  powerful  inhibition  is  produced  than 
when  they  are  applied  to  the  vagus  itself 

2.  After  the  administration  of  urari,  stimulation  of  the  vagus  no 
longer  produces  inhibition  of  the  heart,  but  stimulation  in  the  region  of 
the  sinus  venosus  will  still  do  so. 

3.  After  the  administration  of  atropia,  neither  stimulation  of  the  vagus 
nor  of  the  sinus  produces  any  inhibitory  effect.  It  is  therefore  concluded 
that  atropia  paralyses  the  intra-cardiac  inhibitory  apparatus  itself 

4.  Muscarin  and  jaborandi  in  full  doses  produce  exactly  the  same 
effect  which  is  produced  by  powerful  vagus  stimulation,  viz.,  complete 
arrest  during  diastole,  an  effect  which  is  not  prevented  by  the  previous 
administration  of  urari  (which,  as  we  have  seen,  paralyses  the  terminal 
fibres  of  the  vagus,  but  does  not  touch  the  intra-cardiac  inhibitory 
mechanism)  ;  but  which  is  prevented  by  the  previous  administration  of 
atropia  which  paralysis  the  intra-cardiac  inhibitory  mechanism.  Hence 
it  is  concluded  that  muscarin  and  jaborandi  stimulate  the  intra-cardiac 
inhibitory  mechanism. 

Dr  Gaskell's  view  as  to  the  mode  of  action  of  the  vagus  is 
different.  He  has  shown  that  the  action  of  the  vagus  on  the 
cardiac  muscle  is  in  many  respects  identical  with  the  action  of 
a  weak  interrupted  current.  He  believes  that  the  nerve  acts 
directly  upon  the  muscular  fibre  itself,  and  he  argues  that  the 
action  of  atropin,  muscarin,  and  some  of  the  other  cardiac 
poisons  to  which  I  have  referred  above,  can  be  consistently 
explained  upon  this  view.^ 

'Again,'  he  says,  'I  have  shown  clearly  that  the  vagus 
depresses  and  exalts  all  the  different  functions  of  all  the 
different  muscular  tissues  of  the  heart,  whether  the  function  in 
question  is  rhythm,  contraction,  conduction,  tone,  or  excit- 
ability. Also,  I  have  shown  that  depression  of  one  function 
is  not  necessarily  accompanied  by  a  simultaneous  depression 
of  another  function,  and  so  also  with  the  exaltation  of 
function.  Further,  the  exaltation  of  each  function  is  not 
necessarily  dependent  upon  a  previous  depression  ;  in  each 
case   the   primary  effect   may,  under  certain  circumstances,  be 

'  youriial  of  Physiology,  vol.  iv.,  No.  2,  pp.  114,  115,  116. 


36  Diseases  of  the  Heart. 

exaltation  and  not  depression.  Combining  these  two  facts 
together,  we  are  driven  to  accept  one  of  two  alternatives,  either 
the  vagus  contains  a  multiplicity  of  fibres,  which  can  be 
divided  into  two  groups  after  the  fashion  of  Heidenhain, 
I.  Depressors  (Hemmungs-fasern)  ;  2.  Augmentors  (Ver- 
starkungs-fasern) ;  and  further,  each  member  of  each  of  these 
groups  has  again  its  own  special  function,  so  that,  for  instance, 
the  rhythm-inhibiting  nerve  fibre  is  different  in  kind  from  the 
contraction-depressing  fibre,  and  so  on  ;  or  else,  the  same 
trophic  nerve  fibre  produces  all  the  different  effects  observed, 
according  to  the  nature  of  the  muscle,  which  it  supplies,  and 
the  condition  of  that  muscle  at  the  time. 

'  In  this  paper  as  well  as  in  my  previous  paper,  all  the  facts 
have  tended  strongly  to  prove  that  the  vagus  acts  in  the  same 
manner  upon  the  rhythm  of  the  heart,  and  upon  the  force  of 
its  contractions,  so  that  if  separate  inhibitory  and  accelerator 
nerve  fibres  exist  for  the  one,  separate  depressor  and  aug- 
mentor  fibres  must  exist  for  the  other.  If,  therefore,  it  can 
be  shown  that  such  diminution  and  augmentation  of  the 
strength  of  the  contractions  are  due  not  to  different  influences 
reaching  the  muscle,  but  to  the  same  influence  affecting  the 
muscle  when  its  conditions  are  different,  then  it  is,  to  say  the 
least,  highly  probable  that  slowing  and  acceleration  are  also 
due,  not  to  different  nerve  fibres,  but  to  the  action  of  the  same 
nerve  fibre  under  different  circumstances.  In  the  frog,  as  I 
have  previously  pointed  out,  such  a  complete  gradation  exists 
between  a  primary  excessive  diminution  of  the  contractions 
and  a  primary  augmentation  in  consequence  of  nerve  stimula- 
tion, as  to  render  the  hypothesis  that  such  curves  depend 
upon  the  simultaneous  stimulation  of  two  antagonistic  nerve 
fibres  very  improbable.  I  have  now  proved  in  addition,  that 
a  weak  interrupted  current  applied  to  the  smallest  strip  of 
cardiac  muscle  produces  the  same  two  opposite  effects,  and 
that  here  the  depressing  effect  may  be  removed  and  the  aug- 
menting alone  remain,  when  the  condition  of  the  muscle  is 
altered  by  the  application  of  atropin.  In  order,  therefore,  to 
still  hold  to  the  view  of  specific  nerve  fibres  acting  in  opposite 
directions  upon  the  force  of  the  contractions,  it  is  necessary  to 


The    Trophic  Action  of  the  Vagus,  37 

assume,  not  only  that  those  nerve  fibres  possess  opposite 
quahties  up  to  their  very  termination  in  the  muscle,  but 
that  even  when  the  muscle  itself  is  stimulated,  the  relative 
action  of  these  two  sets  of  nerves  still  holds  its  ground.  In 
addition,  atropin  would  have  to  be  considered  as  acting  upon 
these  two  sets  of  nerve  endings,  and  not  upon  the  muscle, 
paralysing  the  depressor  nerve  endings  before  those  of  the 
augmentor  nerves.  The  experiments  of  Luchsinger  and  Szpil- 
man,^  which  lead  them  to  the  conclusion  that  atropin  has  a 
special  action  upon  unstriped  muscle  fibre,  those  of  Bow- 
ditch,  already  referred  to,  and  my  own,  all  point  to  the  con- 
clusion that  atropin  affects  the  cardiac  muscle  directly  in 
consequence  of  its  affinity  to  unstriped  muscle  fibre.  The 
whole  evidence  goes  to  show  that  the  vagus  is  a  constructive 
and  not  a  destructive  nerve,  that  the  initial  depression  of 
function  is  not  of  the  nature  of  exhaustion,  but  is  preliminary 
to  a  greater  functional  activity.  The  phenomenon  presented 
by  the  muscular  tissue  of  the  frog  and  tortoise  under  the 
influence  of  an  induced  current,  is  of  exactly  the  same  nature 
as  that  seen  in  the  muscle  of  the  snail's  heart  (as  pointed  out  by 
Foster  and  Dew-Smith)  when  a  constant  or  weak  interrupted 
current  is  sent  through  it.  In  both  cases  augmentation  of 
function  occurs  as  well  as  depression  ;  in  the  one  case  the 
evidence  is  as  strong  in  favour  of  special  inhibitory  and 
accelerator  nerves  as  in  the  other.  Clearly,  in  the  case  of  the 
snail,  it  is  simply  impossible,  as  Foster  has  said,  to  explain 
such  results  by  the  presence  of  accelerator  and  inhibitory 
fibres  in  every  strip  of  muscular  tissue,  when,  as  a  matter  of 
fact,  cardiac  nerves  of  any  kind  whatever  have  not  been 
proved  to  exist.  Clearly  also,  whatever  explanation  will  ulti- 
mately be  found  for  the  action  of  the  current  upon  the  mus- 
cular tissue  of  the  snail's  heart,  will  also  explain  the  same 
phenomena  in  the  heart  of  the  frog  and  tortoise.  The  problem 
which  demands  solution  is  essentially.  Why  is  the  condition  of 
the  muscle  ultimately  improved  in  every  one  of  its  functions 
by  the  direct  application  to  it  of  a  continuous  stimulus,  which 

'   Pfliiger's  Archtv.,  vol.  xxvi.  p.  459. 


38  Diseases  of  the  Heart. 

is  not  strong  enough  to  produce  motor  effects?  and  why 
is  that  improvement  of  function  preceded  in  many  cases  by 
a  diminution  of  function  ?  When  these  two  questions  have 
received  a  satisfactory  answer,  it  will  no  longer  be  strange 
that  the  vagus  produces  throughout  two  opposing  effects,  and 
the  action  of  atropin  will  become  clear  ;  then  the  relationship 
between  trophic  and  motor  action  will  be  understood,  and  the 
true  functions  of  the  ganglion  cells  found  in  connection  with 
nerve  fibres  will  be  indicated.  At  present  it  can  only  be  said 
that  the  vagus  is  the  trophic  nerve  of  the  cardiac  muscle,  its 
action  resembling  that  of  a  stimulus  too  weak  to  produce 
motor  effects,  and  therefore  it  is  possible  that  the  function  of 
the  ganglion  cells,  in  the  course  of  the  nerve,  is  to  convert  an 
otherwise  motor  into  a  trophic  nerve.' ^  'This  argument,'  Dr 
Gaskcll  writes  me,  'is  based  upon  experiments  upon  cold- 
blooded animals;  how  far  it  applies  to  the  warm-blooded  I  (Dr 
Gaskell)  do  not  yet  know.  Eichhorst  and  Zander  conclude 
that  the  vagus  in  the  warm-blooded  contains  trophic  fibres.' 

The  action  of  the  sympathetic  upon  the  heart  is  even  less 
clearly  understood  than  the  action  of  the  pneumogastric,  but 
it  is  believed  that  there  exists  in  the  medulla  oblongata  (or 
possibly  above  it),  a  centre,  stimulation  of  which  produces 
increased  frequency  of  the  heart's  beat,  and  it  is  supposed 
that  this  accelerator,  or  cardiac-motor  centre,  as  it  is  some- 
times called,  may  be  stimulated,  i.e.,  the  frequency  of  the 
heart's  beat  may  be  increased  either  by  direct  or  reflex 
stimuli.  The  influences  which  throw  this  centre  into  action 
have  not  been  very  accurately  ascertained,  but  it  is  probable 
that  emotion  excites  the  heart  through  the  agency  of  the 
accelerator  nerves  ;  while  diminished  blood  pressure  within 
the  cranium  is  supposed  to  stimulate  them. 

Impulses  generated  in  this  centre,  the  action  of  which,  be 
it  observed,  is  supposed  to  be  intermittent  (and  in  this 
respect  to  differ  from  the  action  of  the  cardio-inhibitory 
centre,  which  is  supposed  to  be  constant),  appear  to  pass 
down  the  lateral  column  of  the  cord  to  the  lower  end  of  the 

^  Journal  of  Physiology,  vol.  iv.  p.  121. 


The  Action  of  the  Sympathetic  on  the  Heart.        39 

cervical  region,  whence  they  pass  through  the  nervi  com- 
municantes,  to  the  (?)  middle  and  inferior  cervical  ganglia  of 
the  sympathetic,  and  thence  to  the  heart. 

According  to  Prof.  Michael  Foster  the  accelerator  nerves  frequently 
pass  along  the  nerves  accompanying  the  vertebral  artery,  and  reach  the 
heart  through  the  last  cervical  and  first  dorsal  ganglia.' 

It  is  supposed  from  the  long  latent  period  which  elapses 
between  stimulation  of  the  accelerator  and  the  production 
of  its  specific  action  on  the  heart,  that  its  fibres  terminate  in 
an  intermediate  ganglionic  apparatus  similar  to  that  which  I 
have  already  described  in  speaking  of  the  termination  of  the 
pneumogastric. 

Now,  although  the  pneumogastric  acts  as  inhibitor,  and 
the  sympathetic  as  accelerator,  it  must  not  be  supposed  that 
their  action  is  directly  antagonistic.  That  such  is  not  the 
case  seems  abundantly  proved  by  physiological  observa- 
tion. Physiologists  have  shown,  says  Dr  M.  Foster,  that  '  if 
during  maximum  stimulation  of  the  accelerator  nerves,  the 
vagus  be  stimulated  even  with  minimum  currents,  inhibition 
is  produced  with  the  same  readiness  as  if  the  accelerator 
nerves  were  not  acting.  Vagus  stimulation  does  not  annul, 
but  appears  simply  to  suspend,  during  its  continuance,  the 
manifestation  of  the  accelerator  action.'  - 

It  may  appear  to  some  that  I  have  entered  into  undue  physiological  detail  in 
dealing  with  this  subject,  but  it  must  be  remembered  that  it  is  only  by  attention 
to  these  minute  physiological  details  that  the  physician  can  hope  to  make  much 
advance  in  cardiac  patholog)',  a  subject  on  which  our  knowledge  of  the  ordinary 
details  of  morbid  anatomy  is  already  so  far  advanced. 

The  relationship  between  the  Heart  and  the  minute 

Blood-vessels. 

In  order  to  conclude  the  description  of  the  innervation  of 

the   heart,  I    must  shortly   direct  attention   to   the   intimate 

relationship  which  exists  between  the  heart  on  the  one  hand 

'  The  middle  and  lower  cervical  ganglia  in  man  appear  to  correspond  to  the 
lower  cervical  and  first  dorsal  ganglia  in  the  rabbit,  through  which  accelerator 
impulses  have  been  proved  to  pass,  as  shown  in  figure  14. 

-    Text  Book  of  Physiology,  Third  edition,  p.  175. 


40  Diseases  of  the  Heart. 

and  the  peripheral  blood-vessels  on  the  other,  and  to  the 
beautiful  self-adjusting  mechanism  by  which  alterations  in 
the  one  are  of  necessity  followed  by  corresponding  changes 
in  the  other. 

\Vc  have  already  seen  the  fundamental  importance  of 
looking  at  the  heart  both  as  a  mechanical  pump  and  as  a 
vital  organ ;  and  another  point  which  I  must  now  insist  upon — 
and  it  is  hardly  of  less  importance  whether  we  are  studying 
the  heart  from  a  physiological,  a  pathological,  or  a  clinical 
point  of  view, — is  the  necessity  of  taking  an  all-round  view, 
so  to  speak,  of  the  circulation.  Indeed  it  is  essential  to 
remember  that  the  heart  is  only  a  part  of  the  vascular 
mechanism,  and  that  the  condition  of  the  circulation,  and 
consequently  the  condition  of  the  heart  (for  the  organ 
naturally  adapts  itself  to  the  amount  and  kind  of  work  which 
it  has  to  perform)  depend  in  no  small  degree  upon  the 
condition  of  the  peripheral  resistance,  which  is  in  its  turn 
mainly  due  to  the  obstruction  which  the  blood  meets  with, 
in  passing  through  the  minute  arteries. 

In  conditions  of  health,  the  minute  arteries  are  always 
more  or  less  constricted  in  consequence  of  a  permanent  con- 
traction of  their  middle  or  muscular  coats,  and  it  is  to  this 
'  tonic '  contraction  that  the  peripheral  resistance  is  in  great 
part  due.  [The  peripheral  resistance  depends  also  upon 
the  facility  with  which  the  blood  passes  through  the 
capillary  system  of  ves.sels  ;  and  since  the  blood  flow 
through  the  capillaries  may  be  influenced  by  alterations  in 
(a)  the  condition  of  the  capillary  walls,  (b)  the  condition 
of  the  tissues  outside  the  capillary  walls,  and  (c)  the 
composition  of  the  blood  itself,  all  of  these  factors  must 
be  taken  into  consideration  as  causes  of  peripheral  resist- 
ance, and  of  variations  in  the  blood  pressure.  In  con- 
ditions of  disease,  variations  in  the  blood  pressure  may 
result  from  alterations  in  the  '  capillary  resistance,'  but 
these  variations  are,  in  my  opinion,  never  so  great,  either 
in  conditions  of  health  or  disease,  as  those  which  are  due 
to  alterations  in  the  condition  of  the  muscular  coat  of  the 
minute  arteries]. 


Relationship  of  Heart  and  Minute  Blood-vessels.     41 

The  degree  of  constriction  is  constantly  undergoing  varia- 
tions even  in  health,  and  is  subject  to  marked  alterations  in 
some  diseased  conditions  ;  hence  the  amount  of  resistance 
which  the  heart  has  to  overcome  in  forcing  the  blood  into 
the  capillaries,  is  constantly  changing ;  and  to  meet  sudden 
variations  of  this  description  a  delicate  self-adjusting  nervous 
mechanism  is  provided.  But  in  order  that  this  part  of  our 
subject  may  be  properly  understood,  I  must  now  describe 
the  mechanism  by  means  of  which  the  arterial  'tone'  is 
regulated.     There  seems  good  reason  to  believe  :  — 

(i)  That  the  tonic  constriction  of  the  muscular  coats  of 
the  minute  arteries  is  (immediately)  due  to  the  presence  of  a 
peripheral  neuro-muscular  or  (purely)  muscular  apparatus, 
which  may  be  thrown  into  action  by  local  stimuli,  the  most 
important  of  which  is  the  blood  pressure. 


The  peripheral  mechanism  concerned  in  this  maintenance  of  arterial 
'  tone '  probably  bears  a  close  resemblance  to  the  peripheral  mechanism 
concerned  in  the  production  of  the  rhythmical  movements  of  the  heart. 

Ganglionic  masses  can  be  demonstrated  in  the  walls  of  many  of  the 
minute  blood-vessels,  and  it  has  been  by  some  authorities  supposed  that 
the  blood  pressure  produces  stimulation  of  the  muscular  coats  of  these 
vessels  in  a  reflex  manner  (see  fig.  17)  ;  but  in  many  vessels  {e.g.  those 
in  the  skin  and  muscle)  no  such  ganglionic  masses  have  as  yet  been 
demonstrated,  and  in  their  case  we  must  conclude  that  the  contraction  of 
their  muscular  coats  is  due  to  direct  stimulation  of  the  muscular  fibre 
itself,  or  of  the  terminal  vaso-motor  filaments  which  are  distributed  to  it. 

The  view,  which  supposes  that  the  muscular  fibre  is  itself  stimulated 
by  the  blood-pressure,  is  probably  the  correct  one. 


(2)  That  the  action  of  this  peripheral  neuro-muscular  or 
purely  muscular  mechanism  is,  under  ordinary  circumstances, 
maintained  and  regulated  by  impulses  which  are  being  con- 
stantly  sent  to  it  from  centres  (vaso-constrictor  centres)  in 
the  medulla  and  spinal  cord,  through  the  vaso-motor  nerves ; 
and  that  the  action  of  these  vaso-constrictor  centres  may  be 
increased  or  diminished  both  by  direct  stimulation  or  in  a 
reflex  manner.  In  other  words,  the  calibre  of  the  minute 
arteries,    and    therefore    the    peripheral    resistance    may    be 


42  Diseases  of  the  Heart. 

increased   or  diminished   by   central    and    peripheral    causes 
(stimuli). 


Fig.  15. — Diagrammatic  representation  of  the  reflex  mechanism,  by  which  (it  has 
been  theorised)  the  muscular  coat  of  the  blood-vessels  is  tkrowti  into  contrac- 
tion, under  the  influence  of  the  blood-pressure. 

E'  E,  Endothelium;  B,  the  blood  in  the  blood-vessel;  M,  the  muscular  coat  of 
the  artery  ;  g,  ganglion  cell — the  reflex  centre  ;  n,  sensory  nerve  fibre,  conducting 
the  impression  generated  by  the  blood  pressure  on  the  sensory  nerve  terminations 
in  the  wall  of  the  vessel  to  the  reflex  centre  ;  n',  motor  nerve  fibril  conducting  the 
impulse  from  the  reflex  centre  to  the  muscle. 

The  vaso-motor  {i.e.  vaso-constrictor)  centre  of  the  medulla,  which  is 
probably  bilateral,  is  situated  immediately  above  the  calamus  scriptorius, 
and  extends  for  some  distance  into  the  pons  (to  i  or  2  m  m.  below  the 
corpora  quadrigemina).  The  conducting  fibres  proceeding  from  it  are 
believed  to  pass  through  the  lateral  columns  of  the  spinal  cord,  and  to 
proceed  to  the  blood-vessels  chiefly  through  the  sympathetic  system  of 
nerves.  The  vaso-motor  centre  of  the  medulla  probably  regulates  the 
vascular  system  of  the  abdomen,  the  arteries  of  the  skin  and  muscles 
being  probably  mainly  supplied  by  vaso-constrictor  fibres  proceeding 
from  the  vaso-motor  centres  in  the  spinal  cord.  The  exact  position  of 
these  spinal  centres  is  not  ascertained. 

The  action  of  the  vaso-motor  {i.e.  vaso-constrictor)  centres,  which, 
it  will  be  remembered,  is  supposed  to  be  constant,  may  probably  be 
intensified  by  : — 

(a)  Increased  blood  pressure  within  the  cranium,  and  local  irritative 
lesions  of  the  medulla. 

(b)  Impressions  proceeding  from  the  cerebrum. 

(c)  Impressions  proceeding  from  the  periphery.  It  has  been  ex- 
perimentally proved  that  irritation  of  any  afferent  (sensory)  nerve,  such 
as  the  sciatic,  will   produce   constriction    of  the   minute   blood   vessels 


Relationship  of  Heart  and  Minute  Blood-vessels.     43 

(especially  those  of  the  abdomen)  and  increased  blood  pressure,  presum- 
ably by  reflexly  stimulating  the  vaso-motor  centre  in  the  medulla. 

(3)  That  the  action  of  the  peripheral  neuro-muscular 
mechanism  may  be  inhibited  by  nervous  impulses  passing  to 
it  from  certain  centres  in  the  medulla,  and  (?)  spinal  cord, 
through  the  vaso-dilator  nerves  ;  and  that  the  action  of  the 
vaso-dilator  centres,  which  is  not  constant,  may  be  called 
into  play  by  central  and  reflex  stimulation. 

The  calibre  of  the  minute  arteries  may  therefore  be 
increased,  and  the  blood-pressure  lowered  either  by  inhibi- 
tion of  the  vaso-constrictor,  or  by  stimulation  of  the  vaso- 
dilator centres  in  the  medulla  and  (.'')  spinal  cord.^ 

It  is  not  absolutely  certain  that  a  distinct  and  separate  vaso-dilator 
centre  exists  ;  some  authorities  in  fact  believe  that  the  same  centre  may 
at  one  time  evoke  vaso-constrictor  and  at  another  vaso-dilator  impulses  ; 
but  it  seems  tolerably  well  ascertained  that  there  are  distinct  fibres  for 
the  conduction  of  these  two  sets  of  impressions,  and  for  theoretical  and 
teaching  purposes  it  is  convenient  to  describe  and  represent  a  distinct 
vaso-dilator  centre.  The  exact  course  of  the  vaso-dilator  conductors  in 
the  cord  is  yet  undetermined,  but  it  seems  probable  that  they  pass  down 
in  some  part  of  the  lateral  columns,  and  reach  the  blood-vessels  chiefly 
through  the  cerebro-spinal  (and  not  through  the  sympathetic)  nerves. 
The  vaso-dilator  centre  in  the  medulla  is  chiefly,  if  not  exclusively, 
connected  with  the  vessels  of  the  abdominal  viscera  ;  and  it  is  most 
readily  thrown  into  action  by  stimuli  passing  to  the  medulla  through  the 
depressor  nerve,  and  by  impressions  passing  from  the  abdominal  viscera 
through  the  splanchnics.'-' 

'  It  must  be  remembered  that  the  inhibitory  action  of  the  vaso-dilators  on  a 
peripheral  neuro-muscular  or  muscular  mechanism,  is  theoretical,  and  it  is  not 
definitely  proved.  '  It  is  quite  possible,'  as  Foster  says,  '  that  dilation  may  be 
brought  about  in  different  ways,  in  different  cases,  and  so  also  with  constriction.' 
— A  Text  Book  of  Physiology,  p.  211. 

-  This  description  of  the  action  of  the  vaso-motor  mechanism  is  not  complete. 
It  must  of  course  be  remembered,  that  local  variations  in  the  blood  supply  are 
being  constantly  required  by  the  ever  varying  needs  of  particular  times  and  organs, 
and  that  as  Prof.  M.  Foster  says,  '  the  great  use  of  the  whole  vaso-motor  system  is 
not  to  maintain  a  general  arterial  tone,  but  to  modify  according  to  the  needs  of  the 
economy  the  condition  of  this  or  that  vascular  area '  {A  Text  Book  of  Physiology, 
page  213).  But  in  studying  cardiac  affections  the  changes  in  the  action  of  the 
heart,  which  are  induced  by  local  variations  of  this  description,  may,  for  practical 
purposes,  be  safely  ignored.  Hence  I  have  limited  my  description  to  those 
alterations  of  the  vaso-motor  mechanism  which  are  sufficiently  general  to  produce 
definite  changes  in  the  action  of  the  heart. 


44  Diseases  of  the  Heart. 

Now,  as  I  have  previously  stated,  a  very  striking  dimi- 
nution of  blood  pressure  results  from  stimulation  of  the 
superior  cardiac  branch  of  the  vagus  or  depressor  nerve, 
as  it  has  therefore  been  called.  It  is  obvious,  therefore, 
that  there  is  an  important  connection  between  the  heart 
and  the  vaso-dilator  centre  in  the  medulla,  by  means  of 
which  the  heart  and  peripheral  blood  vessels  are  brought 
into  such  close  physiological  connection,  that  changes 
at  one  end  of  the  circulation,  so  to  speak,  are  at  once 
attended  by  compensatory  changes  at  the  other.  If,  for 
example,  the  arterial  blood  pressure  is  from  any  cause 
suddenly  increased,  a  sudden  strain  is  necessarily  thrown 
upon  the  left  ventricle,  and  it  might  easily  happen  that  the 
resistance  in  front  was  too  great  for  the  force  of  the  pump. 
Under  such  circumstances  paralytic  distention  of  the  left 
ventricle  and  death  would  follow,  if  it  were  not  for  the  fact 
that  the  undue  distention  of  the  cavity  and  the  effort  which 
the  heart  is  making  to  overcome  the  resistance,  produce 
irritation  of  the  terminal  fibres  of  its  sensitive  nerve  (the 
superior  cardiac  or  depressor  nerve),  in  consequence  of  which 
a  powerful  stimulus  is  sent  to  the  vaso  dilator  centre  in 
the  medulla,  with  the  result  that  a  sudden  dilatation,  of  the 
capacious  blood-vessels  of  the  abdomen,  occurs,  and  that 
there  is  a  rapid  fall  of  the  blood  pressure.  The  peripheral 
resistance  is  in  this  manner  immediately  diminished,  and 
paralytic  distention  of  the  left  ventricle  prevented.  [Where 
the  arterial  constriction  and  increased  blood  pressure  are 
slowly  and  gradually  established,  compensation  is  effected 
in  a  different  manner,  viz.,  by  the  gradual  increase  in  the 
strength  of  the  pump,  witness  the  hypertrophy  of  the  left 
ventricle,  which  occurs  in  cirrhotic  form  in  Bright's  disease.] 

It  has  been  thought  that  the  vaso-dilator  and  vaso-con- 
strictor  centres  are  also  connected  with  the  cardio-inhibiting 
centre  in  the  medulla ;  and  some  physiologists  have  supposed 
that  reflex  inhibition  of  the  heart  might  be  produced  by  the 
stimulation  of  the  sensitive  nerve  of  the  heart  (superior  cardiac 
nerve),  which  presumably  occurs  in  conditions  of  over  dis- 
tention of  the  organ.     The  recent  experiments,  however,  of 


Relationship  of  Heart  and  Minnie  Blood-vessels.     45 

Ludwig  and  Luchsinger,  and  of  Sevvall  and  Donaldson,  seem 
to  prove  that  this  is  not  the  case,  and  that  increased  blood- 
pressure  within  the  heart,  as  a  whole,  generally  weakens  the 
inhibitory  influence  of  the  vagus.  The  last  two  observers, 
however,  conclude  '  that  changes  of  intra-cardiac  pressure,  ivJien 
experienced  by  the  ventricle  alone'  (no  italics  in  the  original), '  are 
without  effect  on  the  cardio-inhibitory  function  of  the  vagus.' ^ 
Possibly,  therefore,  when  the  ventricles  only  are  over-dis- 
tended, some  reflex  inhibition  may  occur  ;  but,  even  if  it  does 
occur,  it  certainly  must  be  temporary  and  slight,  for  the  main 
effect  of  stimulation  of  the  sensitive  nerve  of  the  heart  is 
reflex  stimulation  of  the  vaso-dilator  centre,  and  consequent 
diminution  of  blood-pressure  throughout  the  body  ;  and  dimi- 
nished blood-pressure,  as  we  have  previously  seen,  tends  to 
lessen  rather  than  to  increase,  the  inhibitory  action  of  the 
vagus. 

So  again,  in  some  cases  of  sudden  palpitation,  the  rise  in 
blood  pressure,  which  would  necessarily  be  produced  by  the 
excessive  action  of  the  muscular  pump,  is  possibly  prevented 
by  the  stimulation  of  the  cardio-inhibitory  centre.  Vice  versa, 
if  from  any  cause  the  general  blood  pressure  is  suddenly 
diminished,  the  restraining  influence  of  the  cardio-inhibitory 
centre  is  removed,  and  the  rapidity  of  the  heart's  action  is 
increased — and  the  fall  in  blood  pressure  is  to  some  extent 
at  least  counteracted. 

'  Journal  of  Physiology,  vol.  iii.  p.  363. 


^6  Diseases  of  the  Heart. 


CHAPTER    II. 

GENERAL  PATHOLOGY  OF  THE  HEART. 

Having  directed  attention  to  some  of  the  more  important 
problems  connected  with  the  physiology  of  the  heart,  I  will 
now  briefly  sketch  the  general  pathology^  of  the  organ.  In 
considering  the  pathology  of  the  heart,  it  is  important  to 
remember  that  it  is  a  composite  anatomical  structure,  and 
that  it  may  be  said  to  consist  of  three  distinct  parts,  viz.  :— 

1.  The  pericardium. 

2.  The  muscular  substance  or  myocardium. 

3.  The  endocardium. 

The  affections  of  the  heart  are  €\\\\&x  functional  ox  organic; 
and  I  must  now  briefly  describe  the  characteristic  features  of 
each  of  these  great  groups  of  conditions.^ 

The  Functional  Affections  of  the  Heart. 

The  main  characteristics  of  the  purely  functional^  affec- 
tions of  the  heart  are  as  follows  : — 

(I.)  They  have  no  distinct  morbid  anatomy  ;  in  other 
words,  in  the  purely  functional  disorders  no  changes  are  to 
be  found  after  death  in  the  heart  itself. 

'  The  special  pathology  and  morbid  anatomy  of  the  individual  diseases  which 
aflfect  the  heart,  will  be  more  conveniently  considered  when  I  come  to  treat  of  the 
individual  affections  in  detail. 

^  The  distinction  of  organic  and  functional  disease.  In  cases  of  organic  disease 
distinct  structural  changes  are  found  after  death,  but  in  functional  disorders  no 
such  changes  can  be  demonstrated.  It  is  impossible,  however,  to  draw  a  sharp 
and  absolute  line  of  distinction  between  these  two  conditions,  for  every  functional 
derangement  does  without  doubt  depend  upon  histological  or  chemical  changes  in 
the  anatomical  elements  of  the  affected  part,  and  it  is  probable  that  as  our  means 
of  investigation  become  more  minute,  many  of  the  so-called  functional  affections 
will  be  proved  to  be  organic. 

^  The  purely  functional  affections,  in  which  there  is  no  distinct  morbid 
anatomy,  are  practically  synonymous  with  the  neurotic  affections  of  the  heart. 


General  Pathology  of  the  Heart.  47 

(2.)  They  are  often  sudden  in  their  onset,  and  usually 
temporary  in  their  duration  ;  they  seldom  if  ever  destro}' 
life,  and  they  are  not,  as  a  rule,  followed  by  any  permanent 
injurious  effects. 

Some  of  the  so-called  functional  affections  do  occasionally  result  in 
organic  disease  ;  in  exophthalmic  goitre,  for  example,  palpitation  and 
accelerated  action  of  the  heart  are  prominent  symptoms,  and  are  for  a 
time,  at  least,  unattended  by  any  perceptible  physical  alterations  of  the 
organ,  but  hypertrophy,  and  more  especially  dilatation,  do  in  many  cases 
ultimately  occur. 

(3.)  They  are,  as  a  rule,  due  to  derangement  of  the  nervous 
mechanism  of  the  heart  ;  and  the  primary  cause  is  very  often 
located  in  some  distant  organ. 

In  some  cases,  the  primary  lesion  (if  we  may  use  the  term 
in  connection  with  hysteria,  hypochondriasis,  etc.)  is  cerebral. 
Under  this  head  are  included  the  derangements  of  the  heart 
which  are  so  frequently  met  with  in  hysteria,  hypochondriasis, 
and  the  like. 

In  others,  the  cervical  portion  of  the  spinal  cord  is  the  part 
at  fault.  Palpitation  and  extreme  rapidity  of  the  heart's 
action  are  occasionally  met  with,  for  example,  in  cases  of 
myelitis  and  locomotor  ataxy. 

In  a  third  group  of  cases,  the  primary  lesion  is  situated  in 
the  cervical  sympathetic ;  and  in  this  group  we  are  probably 
right  in  placing  the  derangements  of  the  heart,  which  are 
such  striking  symptoms  in  the  affection  termed  exophthalmic 
goitre. 

In  a  fourth  group,  the  derangement  of  the  heart  is  due  to 
reflex  irritation,  the  primary  cause  being  situated  in  some 
peripheral  organ,  such  as  the  uterus  or  ovary. 

While  in  other  cases,  the  intra-cardiac  nervous  mechanism 
itself,  or  the  muscular  fibres,  are  directly  affected  ;  the  palpi- 
tation, irregular  action,  etc.,  which  result  from  the  use  of 
some  drugs,  should  probably  be  included  under  this  head. 

(4.)  The  symptoms  are  usually  referred  to  the  heart  itself, 
and  consist  of  uneasy  sensations,  such  as  pain  and  palpitation. 
There  are  seldom  any  symptoms  resulting  from  mechanical 
derangement  of  the  circulation. 


4 8  Diseases  of  the  Heart. 

The  Organic  Diseases  of  the  Heart. 
The  chief  characteristics  of  the  organic   diseases  of  the 
heart  are  as  follows  . — 

1.  They  have  a  distinct  morbid  anatomy. 

2.  They  are  both  acute  and  chronic  ;  they  are  often  per- 
manent, or  are  usually  followed  by  permanent  structural 
defects ;  they  frequently  shorten,  and  often  destroy  life. 

3.  They  may  affect  either  the  pericardium,  myocardium, 
or  endocardium,  in  many  cases  all  three  structures  being 
involved. 

4.  Their  mode  of  origin  is  various,  but  the  following  main 
groups  may  be  described  : — 

A.  In  some  cases  the  disease  is /nw^n'/j^  mnZ/rtc.  Under 
this  head  are  included  : — 

(rt.)  The  congenital  malformations  and  imperfections,  such 
as  congenital  stenosis  of  the  pulmonary  orifice  and  patency  of 
the  foramen  ovale. 

{b)  The  mechanical  ruptures  of  the  valves  which  some- 
times, though  rarely,  occur  independently  of  any  previous 
cardiac  disease.^ 

{c)  Primary  new  growths  of  the  heart,  such  as  primary 
cancer  and  primary  sarcoma.  These  cases  are  extremely 
rare. 

{d)  Primary  (idiopathic)  inflammations  of  the  heart,  e.g., 
primary  idiopathic  pericarditis,  primary  idiopathic  endocar- 
ditis, primary  idiopathic  myocarditis.  These  conditions  are 
extremely  rare,  but  they  are  occasionally  met  with.  In  many 
cases  these  so-called  primary  idiopathic  inflammations  are  in 
reality  rheumatic  ;  cases  of  pericarditis  are,  for  example,  occa- 
sionally met  with,  in  which  the  cardiac  inflammation  is  fol- 
lowed, instead  of  being  preceded,  by  swelling  of  the  joints 
and  the  other  symptoms  of  acute  rheumatism. 

'  In  the  large  proportion  of  cases  of  rupture  of  the  valves,  which  occur  during 
violent  effort,  mental  agitation,  and  the  like,  the  valve,  which  gives  way,  is  not 
absolutely  healthy,  but  has  been  weakened  by  previous  disease. 


General  Pathology  of  tJie  Heart.  49 

(e)  The  local  softenings,  dilatations,  and  ruptures  of  the 
muscular  substance  which  result  from  disease  of  the  coronary 
arteries.^ 

B.  In  others,  the  cardiac  disease  is  part  and  parcel  of 
a  general  affection. 

Under  this  head  are  included  : — 

ia)  The  inflammations  of  the  pericardium,  of  the  endo- 
cardium, and  of  the  myocardium,  which  occur  in  the  course 
of  rheumatic  fever,  scarlet  fever,  Bright's  disease,  and  many 
other  general  affections. 

{b}j  The  softening  and  degeneration  of  the  cardiac  muscle 
which  occur  in  cases  of  prolonged  high  temperature  (pyrexia), 
notably  in  typhus. 

(c.)  The  fatty  degeneration  of  the  heart,  which  is  associated 
with  general  fatty  changes  throughout  the  body  ;  and  the 
fatty  degeneration  which  is  met  with  in  conditions  of  ansemia, 
notably  in  the  so-called  progressive  pernicious  or  idiopathic 
variety. 

{d.)  The  waxy  degeneration  of  the  cardiac  muscle,  which 
is  occasionally  met  with  in  the  course  of  general  waxy  disease, 
but  which  is  of  little  practical  importance. 

(^.)  The  ulcerative  form  of  endocarditis,  which  is  in  some 
cases  closely  allied  to  pyaemia,  and  in  which  the  cardiac  af- 
fection, though  undoubtedly  the  most  prominent  and  central 
(or  local)  lesion,  is,  in  many  cases,  only  a  local  manifes- 
tation of  a  general  septic  condition. 

(/!)  The  gummatous  affections  of  the  heart,  which  are 
occasionally  seen  in  tertiary  syphilis. 

{g)  The  hypertrophy  of  the  left  ventricle,  that  results 
from  obstructed  arterial  circulation,  and  which  is  seen  in  its 
most  typical  form  in  the  cirrhotic  form  of  chronic  Bright's 
disease  ;  and  the  dilatation  and  hypertrophy  of  the  right 
ventricle,  which  result  from  obstructed  pulmonary  circulation, 

*  Although  I  have  placed  these  cases  under  the  primary  affections  of  the  heart, 
it  must  be  remembered  that  the  disease  of  the  coronary  arteries,  which  gives 
rise  to  them,  is  usually  part  and  parcel  of  a  general  arterial  affection  {e.g.  atheroma). 
From  this  point  of  view,  therefore,  we  might  include  local  softenings,  etc.,  in 
the  second  great  group  of  cases. 

D 


50  Diseases  of  the  Heart. 

notably    in    connection    with    emphysema,    cirrhosis    of    the 
lung,   and    the    pulmonary    congestion    produced    by    mitral 

lesions. 

Many  of  the  chronic  affections  of  the  heart,  which  at  first 
sight  appear  to  be  primarily  cardiac,  i.e.  to  originate  in 
the  heart  itself,  should  be  included  in  this  group.  Chronic 
valvular  lesions,  for  example,  sometimes  owe  their  origin  to  a 
previous  attack  of  rheumatic  fever  and  endocarditis.  Fibroid 
degeneration,  too,  often  results  from  a  previous  myocarditis  ; 
while  the  rare  condition,  aneurism  of  the  heart,  is  usually  pro- 
duced by  a  local  fibroid  change,  which  in  its  turn  may  have 
resulted  from  a  previous  myocarditis.  In  other  cases,  valvular 
lesions  (aortic  valvular  lesions  more  particularly)  are  due  to 
atheromatous  changes  at  the  base  of  the  aorta,  which  are  part 
and  parcel  of  a  general  arterial  disease. 

C.  In  a  third  group  of  cases  the  disease  of  the  heart  is 
due  to  extension  to  the  heart  of  a  morbid  process  which  has 
its  original  seat  in  some  other  organ.  The  extension  may 
take  place — 

(rt.)  By  direct  continuity  of  tissue,  as,  for  example,  in  those 
cases  in  which  a  pericarditis  results  from  an  inflammation  of 
the  pleura,  or  in  which  a  mediastinal  growth,  a  lympho-sar- 
coma,  for  instance,  makes  its  way  through  the  pericardium 
and  involves  the  heart. 

{b.)  Indirectly  through  the  veins  or  lymphatics,  as  in  those 
cases  in  which  secondary  tubercles,  abscesses,  cancers,  or 
hydatids  form  in  the  substance  of  the  heart  or  in  the  peri- 
cardium, the  infective  particles  being  carried  to  the  heart  from 
the  lung  or  some  other  more  distant  organ. 

5.  The  most  prominent  symptoms  (dropsy,  cough,  short- 
ness of  breath,  etc.)  are  generally  due  to  derangement  of  the 
venous  or  arterial  circulation  of  distant  parts  or  organs  ;  the 
symptoms,  referred  to  the  heart  itself,  being  in  most  cases 
comparatively  insignificant. 

Now,  organic  lesions  of  the  heart  chiefly  affect  the  circula- 
tion in  two  ways,  viz. : — 


General  PatJiology  of  the  Heart.  5  i 

A.  By  impairing  the  force  of  the  cardiac  muscle  {cardiac 
pump). 

Lesions,  such  as  fatty,  fibroid  degeneration,  etc.,  which 
weaken  the  cardiac  muscle,  must  of  course  impair  its  '  driving ' 
power,  and  of  necessity  produce  retardation  of  the  circula- 
tion. Lesions  of  this  description  usually  involve  both  sides  of 
the  heart  (both  the  right  and  left  hearts),  and  affect  more 
particularly  the  muscular  walls  of  the  ventricles.  When  the 
strength  of  the  left  ventricle  is  impaired,  the  amount  of 
blood  pumped  into  the  arterial  system  is  less  than  normal, 
while  the  left  auricle,  the  lungs,  the  right  heart,  and  the 
systemic  venous  circulation  become  over-distcndcd,  and  the 
rapidity  of  the  whole  circulation  is  decreased.  When  again 
the  wall  of  the  right  ventricle  is  weakened,  the  amount  of 
blood  supplied  to  the  lungs,  left  side  of  the  heart  and  systemic 
arterial  circulation  is  deficient,  while  the  systemic  venous 
circulation  is  over-distended. 

It  is  important,  too,  to  remember  that  when  the  cardiac 
walls  are  weakened,  the  venous  ostia  (mitral  and  tricuspid 
orifices)  are  less  firmly  closed  than  in  health,  and  a  leakage 
through  these  orifices  is  apt  to  take  place.  This  is  probably 
the  chief  cause  of  the  mitral  regurgitation  which  occurs  in 
chlorosis  and  many  other  conditions ;  and  this  form  of  incom- 
petence we  may  conveniently  term  '  muscularl  i.e.  incom- 
petence due  to  defective  muscular  closure  of  the  valvular 
orifice. 

Then  again,  when  the  cardiac  walls  are  weakened,  the 
blood  pressure,  which  in  conditions  of  health  is  opposed  by 
the  elastic  resistance  of  the  cardiac  muscle,  readily  produces 
dilatation  of  the  cardiac  cavities,  and  this  condition,  i.e. 
dilatation,  materially  adds  to  the  difficulties  of  the  circula- 
tion, for  the  following  reasons  : — 

(a)  In  proportion  as  the  dilatation  increases,  the  walls  of 
the  cavity  become  thinner,  and  therefore  weaker. 

{b)  The  greater  the  amount  of  blood  which  the  cavity 
contains,  the  greater  the  amount  of  force  required  to  empty 
it. 

(r.)  Dilatation  of  the  ventricles,  by  preventing  the  perfect 


52  Diseases  of  the  Heart. 

closure  of  the  auricula-ventricular  valves  permits  of  regurgi- 
tation, and  to  this  condition  the  term  '  relative  incompetence'  is 
usually  applied.  It  is  probable,  however,  that  in  many  cases 
of  dilatation,  defective  muscular  closure  (the  condition  which 
produces  '  miiscidar  incompetence',  as  I  term  it)  is  a  more 
important  cause  of  regurgitation  than  the  actual  stretching  of 
the  valvular  orifice  itself. 

In  dilatation,  then,  the  muscular  wall  is  not  only  weaker 
than  in  health,  but  a  greater  amount  of  work  is  actually  de- 
manded of  it ;  and  the  circulation  may  be  still  further  embar- 
rassed by  regurgitation  through  the  auriculo-ventricularorifices. 

It  is  extremely  important  to  remember  that  the  re- 
gurgitation which  results  from  '  defective  muscular  closure,' 
and  from  '  relative  incompetence,'  is  not  necessarily  a  perma- 
nent condition.  Indeed  in  many  cases  we  can,  by  appropriate 
treatment,  restore  the  cardiac  muscle  to  its  previously  healthy 
state,  and  with  the  restoration  of  the  cardiac  muscle  the 
regurgitation  necessarily  disappears. 

The  condition,  therefore,  of  the  cardiac  muscle,  and  the 
presence  or  absence  of  dilatation,  are  points  of  the  greatest 
practical  importance.  Indeed,  as  we  shall  afterwards  see,  the 
prognosis  is  largely  based  upon  the  condition  of  the  heart  in 
these  respects  ;  and  the  treatment  of  cardiac  affections  is,  to  a 
great  extent,  directed  to  maintaining  the  cardiac  muscle  in  a 
sound  and  healthy  state. 

B.  By  producing  structural  alterations  in  the  valvular 
orifices,  and  valve  flaps,  ivhich  interfere  tvith  the  valvular 
mechanism,  and  prevent  the  steady  onward  flow  of  blood  in  the 
natural  course  of  the  circulation. 

These  alterations  constitute  the  great  group  of  valvular 
lesions  properly  so  called.  They  are  usually  permanent  and 
incurable.  They  consist  of  adhesions,  thickenings,  contrac- 
tions, and  ulcerations  of  the  valve-flaps  and  adjacent  parts, 
in  consequence  of  which,  narrowing  {stenosis)  of  the  valvular 
orifice,  or  imperfect  closure  of  the  valvular  apparatus  {incom- 
petence^ is  produced.  The  two  conditions  (stenosis  and  incom- 
petence) are  very  generally  combined  ;  in  some  cases  stenosis, 
in  others  incompetence  being  the  more  prominent. 


General  Pathology  of  the  Heart.  53 

Both  conditions  (stenosis  and  incompetence)  interfere  with 
the  steady  onward  flow  of  blood  in  the  normal  direction,  and 
produce  diminished  supply  of  blood  to  the  parts  in  front  of 
the  lesion  and  vascular  engorgement  of  the  parts  behind.  But 
the  manner  in  which  these  effects  are  produced  differs  some- 
what in  the  two  cases.  In  stenosis  the  obstruction  \% passive, 
the  blood  simply  stagnating,  as  it  were,  in  the  cavities  of  the 
heart  and  parts  of  the  circulation  behind  the  '  block  ; '  while 
in  incompetence  the  obstruction  may  be  termed  active,  for  it 
is  due  to  a  '  backwash'  or  regurgitant  current,  which  presses 
back,  as  it  were,  and  arrests  the  advance  of  the  blood  column 
into  the  cavity  of  the  heart,  which  is  situated  immediately 
behind  the  seat  of  the  lesion. 

But  further,  the  regurgitant  current,  passing  as  it  does 
with  considerable  force  into  a  cavity,  the  walls  of  which  are 
relaxed  and  flaccid,  has  a  stronger  tendency  to  produce  di- 
latation of  that  cavity  than  simple  passive  obstruction  has 
— witness  the  condition  of  the  left  ventricle  in  aortic  stenosis 
and  incompetence  respectively  ;  and  dilatation  adds,  as  we 
have  already  seen,  very  materially  to  the  difficulties  of  the 
circulation. 

Now,  from  what  I  have  said,  it  might  be  supposed  that 
every  structural  alteration  which  produces  either  stenosis  or 
incompetence  of  a  valvular  orifice,  is  necessarily  attended  by 
symptoms  due  to  disturbance  of  the  circulation  ;  and  such 
in  truth  would  be  the  case,  if  it  were  not  for  the  fact,  that 
nature  adapts  herself  to  the  altered  condition  of  things  ;  and 
that  certain  secondary  changes  are  gradually  established,  by 
virtue  of  which  the  bad  effects  of  derangement  of  the  circula- 
tion are  resisted,  and  by  means  of  which  the  normal  balance, 
so  to  speak,  of  the  circulation  is  maintained  or  re-established. 
There  is,  in  short,  in  almost  all  cases  of  valvular  defect,  a 
natural  effort  to  compensate  the  lesion,  the  importance  of  which 
in  a  practical  point  of  view,  it  is  impossible  to  over-estimate. 

These  compensatory  changes  consist  of  alterations  in 
the  heart,  the  object  of  which  is  to  restore  and  maintain  the 
balance  of  the  circulation,  and  to  resist  the  injurious  effects 
of  the  lesion  on  the  heart  itself;   and  of  certain  changes  in 


54  Diseases  of  the  HearL 

the  peripheral  tissues,  by  means  of  which  the  injurious  effects 
of  backward  pressure  and  venous  stagnation  are,  to  some 
extent,  prevented. 

The  exact  nature  of  these  compensatory  changes,  which 
depend  upon  (i.)  the  valve  which  is  affected  ;  and  (2.)  the 
manner  in  which  it  is  affected  {i.e.  whether  stenosis  or  incom- 
petence, is  the  chief  lesion),  will  be  more  appropriately  con- 
sidered when  I  come  to  treat  of  the  individual  valvular  lesions 
in  detail ;  but,  speaking  broadly,  I  may  say  that  in  all  valvular 
lesions  compensation  is  chiefly  effected  by  hypertrophy  of  the 
walls  of  the  cardiac  cavity  or  cavities,  which  are  situated 
behind  the  affected  orifice.^ 

When,  for  instance,  the  aortic  orifice  is  contracted,  the 
muscular  wall  of  the  left  ventricle  becomes  thicker,  and  the 
'  driving '  power  of  the  left  heart  being  materially  increased,  a 
larger  quantity  of  blood  is  propelled  in  a  given  time  through 
the  narrowed  orifice  than  could  possibly  have  been  the  case 
in  the  normal  (un-hypertrophied)  condition.  So  again  stenosis 
of  the  mitral  valve  is  followed  by  hypertrophy  of  the  left 
auricle,  but  in  this  case  (the  normal  function  of  the  auricle 
being  passive  rather  than  active,  and  the  resisting  power  of  its 
walls — against  the  blood  pressure — depending  not  only  upon 
the  muscular  tissue  but  also  upon  the  connective  tissue  layers 
of  the  endocardium),  the  hypertrophy  consists  not  only  of  an 
increase  of  the  muscular  wall  of  the  auricle,  but  also  of  thick- 
ening of  its  elastic  tissue  lining.  By  these  means  its  resist- 
ing power  is  materially  strengthened  at  the  same  time  as 
its  propelling  power  is  increased.^  This  increase  of  the  con- 
nective tissue  coat  of  the  auricle  is  (in  proportion  to  the 
amount  of  muscular  hypertrophy)  still  more  marked  in  mitral 

'  Alterations  in  the  frequency  of  the  cardiac  contractions  also  exert  an  important 
compensatory  influence,  more  especially,  as  we  shall  afterwards  see,  in  the  case  of 
aortic  lesions. 

-  The  reader  must  not  suppose  from  this  statement  that  all  fibroid  changes  in  the 
cardiac  walls  add  to  the  resisting  power  of  the  organ.  When  the  muscular  tissue 
of  the  organ  is  replaced  by  fibrous  tissue,  as  it  is  in  fibroid  degeneration,  both  the 
'  driving '  and  resisting  power  of  the  organ  are  diminished.  It  is  only  when  the 
muscular  wall  remains  healthy,  or  is  hypertrophied,  that  an  increase  of  the  fibrous 
tissue  in  the  endocardium  can  possibly  add  to  its  resisting  power. 


General  PatJiology  of  the  Heart.  55 

incompetence,  in  which  condition,  as  we  have  previously  seen, 
increased  resistance  is  necessary  to  counteract  the  dilating 
force  of  the  regurgitant  current,  but  in  which  there  is  no 
obstruction  to  the  passage  of  the  blood  from  the  auricle  to  the 
ventricle.  So  again  in  aortic  regurgitation,  the  forcible  pas- 
sage of  an  abnormally  large  quantity  of  blood  into  the  cavity 
of  the  left  ventricle  during  its  diastole  (from  the  aorta  through 
the  incompetent  valve,  and  from  the  left  auricle  through  the 
mitral  orifice),  produces  over-stimulation  of  the  muscular  fibre, 
in  consequence  of  which,  hypertrophy  of  the  left  ventricle  is 
produced  ;  and  this  for  a  time,  at  least,  is  able  to  counter- 
balance the  bad  effects  of  dilatation,  a  condition  which  is 
produced,  as  we  have  already  seen,  by  the  too  forcible  dis- 
tention of  the  cavity  while  its  walls  are  flaccid  and  relaxed. 

The  hypertrophy,  then,  which  follows  and  accompanies 
valvular  lesions,  is  eminently  beneficial,  though  it  is  not  in  all 
cases  an  unmixed  good  ;  and  I  cannot  insist  too  strongly 
upon  the  immense  importance  of  this  doctrine  of  compensa- 
tion. The  symptoms,  as  we  shall  afterwards  see,  are  trivial, 
or  altogether  absent,  so  long  as  the  compensatory  changes 
are  sufficient  to  balance  the  bad  effects  of  the  lesion  ;  the 
prognosis  is  very  largely  based  upon  the  amount  of  com- 
pensation and  the  capabilities  of  repair  which  are  present ; 
while  the  treatment  is  in  great  part  directed  to  promoting  and 
maintaining  the  hypertrophy  and  other  secondary  changes, 
by  means  of  which  the  balance  of  the  circulation  is  restored 
and  maintained  in  a  comparatively  normal  condition. 

The  amount  of  compensation  which  is  possible  in  any 
given  case,  depends  chiefly  upon  the  following  circumstances  : 

I.   TJie  siiddauiess,  extent,  anel  character  of  the  lesion. 

A  very  extensive  lesion,  which  occurs  suddenly — rupture  of 
the  heart,  for  instance — may  of  course  destroy  life  so  rapidly 
that  compensatory  changes  cannot  possibly  occur. 

Then  again  a  severe  (but  not  immediately  fatal)  lesion 
which  occurs  suddenly,  is  with  difficulty  compensated — rup- 
tures and  ulcerations  of  valves  are  examples. 

In  other  cases,  on  the  contrary,  in  which  the  progress 
of  the  lesion    is   slow  and    gradual,  compensation  is  easily 


56  Diseases  of  the  Heart. 

established,  and  is  very  complete.  In  many  chronic  valvular 
lesions,  for  example,  compensatory  changes  advance  pari 
passu  with  the  morbid  process,  and  for  a  time  at  least,  the 
balance  of  the  circulation  is  so  satisfactorily  maintained,  that 
the  patient  (provided  that  he  lives  a  quiet  and  tranquil  life, 
and  does  not  suddenly  add  to  the  difficulties  of  the  circula- 
tion) may  be  unaware  of  the  existence  of  any  cardiac  defect. 

2.  The  reparative  pozvers  of  the  patient,  and  especially  the 
capabilities  of  compensation  existing  in  the  heart  itself 

3.  The  resisting  power  of  the  tissues,  which  in  its  turn 
depends  upon  the  soundness  and  vitality  of  the  individual 
organs,  and  especially  upon  the  vaso-motor  nerve  tone,  and 
the  vitality  of  the  whole  organism. 

In  young  persons,  where  the  tissues  are  healthy,  and  in 
persons  of  good  nerve  tone  and  tranquil  disposition,  com- 
pensation is  satisfactorily,  and,  for  a  time  at  least,  effectually 
established.  Vice  versa,  in  old  people,  in  persons  whose 
tissues  are  unsound  or  degenerating,  more  especially  in  those 
in  whom  the  nerve  tone  is  bad,  compensation  is,  from  the 
first,  imperfect,  and  the  injurious  effects  of  the  lesion  are 
speedily  manifested  in  the  form  of  symptoms. 

The  condition  of  the  tissues,  then,  as  a  whole,  and  the 
reparative  power  and  vitality  of  the  patient  are  facts  which 
the  practical  physician  must  ever  keep  prominently  in  view. 
Indeed,  we  may  lay  it  down  as  an  axiom,  that  in  looking  at 
cardiac  cases,  zuhether  from  a  pathological  or  a  clinical  point 
of  viezu,  and  more  especially  in  considering  the  prognosis  and 
treatment,  it  is  quite  as  important  (I  might  even  say  that  in 
some  cases  it  is  more  important)  to  look  at  the  condition  of  the 
system  as  a  zvhole,  as  it  is  to  regard  the  condition  of  the  heart  in 
particular.  He  is  in  fact  a  poor  physician  who  concentrates 
his  attention  upon  the  tissue  or  organ  which  is  primarily 
affected  ;  and  this  statement  holds  good  even  should  he 
succeed  in  arriving  at  an  accurate  estimate  of  the  cardiac  or 
other  local  lesion  ;  while  the  best  physician  is  he  who 
accurately  guages  the  nature  and  extent  of  the  local  lesion, 
and  at  the  same  time  takes  a  broad  and  comprehensive  all- 
round  view  of  the  case. 


Clinical  Exajuination  of  Cardiac   Cases.  5 


CHAPTER    III. 

THE  CLINICAL  INVESTIGATION  OF  CASES  OF  CARDIAC  DISEASE- 
METHOD  OF  CASE-TAKING  — SUMMARY  OF  SYMPTOMS  — THE 
PHYSICAL  EXAM  [NATION-INSPECTION— PALPATION— PERCUSSION^ 
AUSCULTATION— THE  USE  OF  THE  SPHYGMOGRAPH. 

Having  considered  some  of  the  most  important  points 
connected  with  the  physiology  and  general  pathology  of  the 
heart,  we  are  now  in  a  position  to  take  up  the  clinical  exami- 
nation of  the  organ.  And  in  order  to  make  this  most  import- 
ant part  of  our  subject  as  clear  and  intelligible  as  possible,  I 
will  first  sketch  out  the  method  of  case-taking,  and  the  plan 
of  examination  which  I  am  in  the  habit  of  employing  in  the 
investigation  of  cases  of  cardiac  disease — and  we  shall,  then, 
be  in  a  position  to  consider  the  symptomatology  and  physical 
examination  in  detail. 

Under  the  head  of  the  physical  examination  I  shall : — 

1.  Describe  the  normal  physical  signs  {i.e.  the  signs 
appreciable  to  the  senses — aided  and  unaided — of  the  phy- 
sician, which  result  from  the  physical  condition  of  the  organ 
in  its  healthy  state),  and  their  mode  of  production. 

2.  Describe  the  pathological  physical  signs  {i.e.  the  signs 
which  result  from  the  physical  condition  of  the  organ  when 
diseased)  and  their  mode  of  production. 

3.  Give  in  a  short  and  summary  manner,  the  leading  facts, 
which  will  enable  us,  in  any  case  in  w^hich  an  abnormal 
physical  sign  is  detected,  to  determine  the  nature  of  the 
lesion  which  is  present ;  for  it  is  important  to  remember  that 
few  physical  signs  are  absolutely  distinctive  (pathognomonic); 
in  fact,  diseased  physical  signs,  such  as  increased  dulness  on 
percussion  over  the  prscordia,  may  be  due  to  several  different 
morbid  conditions. 


58  Diseases  of  the  Heart. 


METHOD  OF  CASE-TAKING. 

A.  PRELIMINARY  FACTS  :— Name— Age— Sex— Married  or  Single- 
Occupation— Full  I'uslal  Address — Date  of  Admission  to  Hospital. 

B.  COMPLAINTS: — (The  Symptoms  which  bring  the  patient  to  consult 
the  physician). 

C.  THE  HISTORY:- 

(i.)  Of  the  Present  Illness: — The  exact  date  of  its  commencement.  The 
exact  mode  of  commencement.  The  supposed  cause  of  the  attack.  The  exact 
character  of  the  symptoms ;  the  order  of  their  appearance ;  and  the  treatment 
which  has  been  adopted,  up  to  the  time  when  the  patient  comes  under  observa- 
tion.    (In  acute  cases  take  the  temperature.) 

(2.)  The  Health  History  prior  to  the  commencement  of  the  present 
attack  : — Especially  a  history  of  disease  or  injury  likely  to  be  followed  by  disease 
of  the  heart.     The  habits,  mode  of  life,  and  general  surroundings  of  the  patient. 

(3.)  The  Family  History: — Especially  the  occurrence  of  heart  affections  or 
of  acute  rheumatism  amongst  near  relatives. 

D.  THE  PRESENT  CONDITION  :— (The  date  at  which  the  examina- 
tion is  made  should  be  stated.) 

(I.)  The  Physiognomy  of  the  Case  :— The  description  of  any  striking 
abnormal  appearances.  The  condition  of  the  superficial  vessels.  The  character 
of  the  breathing.  The  presence  of  subcutaneous  oedema.  The  attitude.  The 
general  state  of  nutrition.     The  facial  expression,  etc. 

(2. )  The  presence  or  absence  of  subjective  symptoms  referred  to  :— 

(a.)  The  Heart  /to'/^'.— (Uneasy  sensations  in  the  region  of  the  heart,  palpita- 
tion, pain,  etc.) 

{b.)  Distant  Organs  or  Parts. — (Symptoms  resulting  from  mechanical  dis- 
turbance of  the  circulation — deficient  supply  of  arterial  blood,  or 
venous  engorgement,  etc.) 

(3.)  The  Physical   Examination  of  the   Heart  and  Circulatory  Organs. 
The  Physical  Examination  of  the  Heart. 

Inspection  of  the  Pracordial  Region. 
Observe : — 

(a.)  Its  form  and  configuration. 
{b.)  The  position,  extent,  and  character  of  the  visible  impulse,  especially  the 

position  of  the  apex  beat, 
(r.)  The  condition  of  the  integument  over  the  precordial  region. 


Method  of  Case-taking.  59 

Palpation  of  the  HcarL 
Note  : — 

[a.)  The  exact  position  of  the  apex  beat. 

{b.)  The  character  of  the  cardiac  contractions  (force,  rhythm,  celerity,  etc.) 
(r. )  The  presence  of  prascordial  thrills  or  friction  fremitus. 
{d. )  The  presence  of  pain  or  tenderness  on  pressure  over  the  praecordia. 

Percussion  of  the  Heart. 
Determine  : — 

(a.)  The  area  of  superficial  or  absolute  dulness. 
(/'. )  The  area  of  deep  or  relative  cardiac  dulness. 

Auscultation  of  the  Heart. 
Determine  : — 

((7.)  The  rhythm  of  the  heart,  whether  regular  or  not. 

{h.)  The  character  of  the  individual  (first  and   second)  sounds   in  the  mitral, 
aortic,  pulmonary,  and  tricuspid  areas,  as  regards  : — 

Loudness  or  intensity. 

Tone  and  purity. 

Reduplications. 

Murmurs, 
(c. )  WTiere  a  murmur  is  present,  observe  : — 

Its  rhythm. 

Its  point  of  differential  maximum  intensity. 

The  direction  in  which  it  is  propagated. 

Its  sound  characters. 

The  Physical  Examination  of  the  Aorta  and  Great  Vessels. 

Inspection. 

The  conformation  of  those  parts  of  the  thorax  and  abdomen  which  are  super- 
ficial to  the  aorta  and  great  vessels,  must  be  observed,  particularly  the  presence  of 
any  prominence,  pulsation,  or  tumour. 

Palpation. 
Determine  : — 

(a)  The  presence  of  any  undue  pulsation  in  the  supra-sternal  notch,  or  of  any 
abnormal  pulsation  in  the  thorax  or  abdomen. 

(b)  The  presence  of  thrills,  tenderness  on  pressure,  etc.,  in  the  course  of  the 
aorta  or  great  vessels. 

Percussion. 
Note  :— 

The  presence  of  dulness  on  percussion  in  the  course  of  the  aorta  or  great 
vessels;  its  exact  extent,  outline,  etc. 

Auscultation. 

Observe  : — 

The  character  of  the  heart  sounds,  and  the  presence  or  absence  of  murmurs 
over  the  course  of  the  aorta  or  great  vessels  (their  rhythm,  direction  of 
propagation,  etc.) 


6o  Diseases  of  the  Heart. 

The  Examination  of  the  Superficial  Arteries. 

Note  the  condition  of  the  superficial  arteries,  such  as  the  carotids,  brachials, 
temporals,  etc.,  by  inspection,  and    if  necessary  by  palpation  and   auscultation  : 
and  particularly  observe  the  condition  oi  t/ie  pulse  {i.e.  the  radial  artery)  : — 
(a.)  By  the  finger  (palpation)  as  regards  :— 
Its  frequency. 
Its  rhythm. 
Its  volume. 

Its  compressibility  or  tension. 
The  special  characters  of  each  pulse  wave  (celerity,  dicrotism,  etc.); 

and  the  condition  of  the  vessel  (in  respect  to  its  fulness)  during   the 
diastole  of  the  ventricle. 
The  condition  of  the  arterial  coats. 

The   comparative   conditions    on    the    two    sides    of    the    body    (i.e.    the 
comparison  of  the  two  radial  arteries). 
{l>.)  By  the  eye  (inspection). 
(c.)  By  the  sphygmograph. 


The  Examination  of  the  Venous  System. 
inspection. 

Note  the  condition  of  the  superficial  veins,  and  particularly  observe  the 
condition  of  the  jugulars  as  regards  fulness,  the  presence  of  pulsation,  etc. 

Auscultation. 

Note  the  presence  or  absence  of  a  venous  hum  in  the  neck,  over  the  orbit, 
Torcular  Herophili,  etc. 

(4.)  The  condition  of  the  Respiratory,  Alimentary,  Genito- Urinary. 
Nervous,  and  Integumentary  Systems. 

E.  THE  DIAGNOSIS. 

F.  THE  PROGNOSIS. 

G.  THE  TREATMENT— Hygienic,  Dietetic,  Medicinal  (general  and 
local). 

H.  THE  SUBSEQUENT  COURSE  OF  EVENTS. 

The  progress  of  the  case  during  the  patient's  stay  in  hospital.  The  mode  of 
termination  of  the  case.  The  date  of  termination.  In  fatal  cases  the  record  of 
the  post-mortem  examination,  and  an  account  (when  necessary)  of  the  subsequent 
microscopical  examination  of  the  tissues  and  organs. 


Symptoms.  6  r 

SUMMARY  OF  THE  CHIEF  SYMPTOMS. 

Age. — Diseases  of  the  heart  may  occur  at  any  age,  but 
some  affections  are  more  common  at  one  period  of  hfe  than 
at  another. 

Childhood. — Congenital  Alalfonnations  are  generally  at- 
tended with  symptoms,  and  are,  therefore,  as  a  rule,  observed 
immediately  or  soon  after  birth.  Many  cases  prove  fatal 
during  the  first  few  weeks  or  months  of  extra-uterine  exist- 
ence ;  and  severe  cases,  which  do  not  die  at  an  early  stage, 
usually  succumb  at  or  about  the  time  of  puberty.  Congenital 
malformations  are,  therefore,  rarely  noticed,  except  on  the 
post-mortem  table,  in  the  adult.^  Acute  inflammations,  more 
especially  endocarditis,  are  sometimes  seen  in  children,  and 
are  probably  of  much  more  frequent  occurrence  than  is 
generally  supposed  ;  and  cases  of  valvular  disease  are  by  no 
means  rare  before  the  age  of  puberty;  mitral  lesions  frequently 
follow  scarlet  fever,  and  mitral  regurgitation  is  present  in  a 
considerable  proportion  of  the  cases  of  chorea. 

Youth  and  Early  Adult  Life. — Functional  affections  of  the 
heart  are  most  common  from  the  age  of  puberty  up  to  the  age 
of  twenty-five  or  thirty,  but  are  also,  of  course,  met  with  in 
later  life.  Acute  inflammations  of  the  heart,  more  especially 
those  forms  which  are  associated  with  rheumatism,  are  also 
most  common  in  early  adult  life.  The  valvular  lesions,  more 
especially  the  lesions  of  the  mitral  valve,  which  so  often  follow 
acute  endocarditis,  are  consequently  of  frequent  occurrence  at 
this  time. 

Active  manhood. — The  lesions  of  the  heart  and  arteries, 
which  are  due  to  strain,  syphilis,  and  drink,  now  begin  to 
appear,  aortic  valvular  lesions  and  aneurisms  being  espe- 
cially prominent.  The  forms  of  disease,  which  are  prevalent 
in  early  adult  life,  also  occur. 

'  Congenital  lesions  of  the  valves  which  have  not  interfered  with  the  circulation, 
and  which  were  not  suspected  during  life,  are  not  unfrequently  discovered  after 
death.  In  cases  of  this  description  the  congenitally  malformed  valve  is  frequently 
the  seat  of  disease  acquired  in  later  life— of  endocarditis,  chronic  valvular  lesions, 
etc. 


62  Diseases  of  the  Heart. 

Later  Adult  Life  and  Old  Age. — Valvular  lesions,  which 
in  some  instances  date  from  a  former  attack  of  acute 
rheumatism,  and  have  been  long  latent,  now  begin  to  be 
actively  manifested  ;  and  all  the  other  lesions  which  depend 
upon  degenerative  changes  either  in  the  heart  or  arteries 
become  prevalent.  Tnie  angina  pectoris  is  seldom  observed 
before  the  age  of  forty  ;  fatty  degeneration  of  the  heart, 
dilatation,  and  valvular  lesions  of  all  kinds,  are  extremely 
common,  and  cause  a  large  proportion  of  the  deaths 
between  the  ages  of  fifty-five  and  sixty.  In  women  the 
period  between  forty-five  and  fifty,  and  in  males  between 
fifty-five  and  sixty,  seems  a  particularly  critical  one.  The 
tendency  to  aortic  valvular  lesions,  aneurism,  and  all  the  other 
cardiac  changes  which  depend  upon  atheroma,  steadily  in- 
creases with  the  age  of  the  individual ;  and  these  affections 
(aneurism,  apoplexy,  etc.)  would  be  still  more  prevalent  if  it 
were  not  for  the  inactive  (strainless)  lives  which  most  old 
people  lead,  the  tendency  to  arterial  rupture  being  in  con- 
sequence reduced  (considering  the  condition  of  the  arteries) 
to  a  minimum. 

Sex. — The  functional  derangements  of  the  heart,  which 
accompany  hysteria  and  anaemia,  and  the  cardiac  affections 
which  are  met  with  in  cJiorea  and  exophthalmic  goitre  are  very 
much  more  common  in  the  female  sex.^  Those  cardiac  affec- 
tions, on  the  contrary,  which  are  due  to  atheroma  and  gout, 
to  strain,  syphilis,  and  alcohol,  are  very  much  more  prevalent 
in  males  ;  aortic  lesions,  aneurisms,  and  true  angina  pectoris 
are  examples  in  point. 

Occupation. — The  occupation  of  the  patient  exercises  a 
very  distinct  influence  in  the  production  of  cardiac  disease. 
Persons  who  are  exposed  to  cold  and  wet,  such  as  washer- 
women, firemen,  cabmen,  etc.,  are  much  more  liable  to  con- 
tract rheumatic  fever,  and  therefore  to  suffer  from  acute 
inflammatory  affections  of  the  heart  and   the  chronic  valvular 

'  Hysteria,   chlorosis,   chorea,    and   exophthahnic  goitre   are    all    much   more 
common  in  females. 


Sympto7ns.  6 


J 


lesions,  which  so  frequently  supervene  upon  acute  endo- 
carditis, than  other  people.  Blacksmiths,  puddlers,  paviors, 
and  all  persons  engaged  in  laborious  occupations,  more  espe- 
cially those  who  have  to  make  sudden  efforts,  and  who  are 
therefore  exposed  to  strain,  are  more  liable  to  atheroma, 
aortic  valvular  lesions,  and  aneurism,  than  other  people. 
Soldiers  and  sailors  are  also  very  often  affected  with  arterial 
disease  probably  because  they  are  much  exposed  to  strain, 
and  because  they  are  more  subject  to  syphilis  than  other 
members  of  the  community,  and  are  also  frequently  addicted 
to  alcoholic  excesses.  The  constriction  of  the  neck  and  chest, 
which  is  produced  by  tight  or  badly  fitting  clothing  and 
accoutrements,  is  probably  also  another  cause  for  the  pre- 
valence of  aneurisms  amongst  soldiers  ;  the  constriction  pro- 
duces a  direct  mechanical  impediment  to  the  circulation, 
which  is  increased  by  any  strain  or  violent  exertion,  such  as 
a  charge  at  'the  double,'  or  a  'forced  march.' 

Complaints. — In  order  to  understand  the  '  complaints  '  of 
the  patient,  it  is  essential  to  remember  that  the  heart  is  a 
vital  organ  as  well  as  a  mechanical  pump.  There  are,  in 
short,  two  great  groups  of  cardiac  symptoms. 

(i)  In  one,  the  symptoms  are  referred  to  the  heart  itself, 
and  depend  upon  the  fact  that  the  patient  is  conscious  of  some 
derangement  in  its  action  as  a  vital  organ.  These  symptoms, 
which  may  for  the  sake  of  convenience  and  description  be 
termed  'vital ;'  or  better,  'subjective  cardiac  sensations',  consist 
of: — uneasy  sensations  in  the  region  of  the  heart;  conscious- 
ness of  excessive  or  disordered  action  (palpitation,  irregu- 
larity, intermittent  action,  and  the  like)  ;  and  in  some  cases, 
severe  pain  in  the  cardiac  region. 

(2)  In  the  other  group,  the  symptoms  are  referred  to  some 
distant  organ  or  part,  and  depend  upon  the  mechanical 
derangements  in  the  circulation  which  are  produced  by  the 
cardiac  lesion  {i.e.  derangement  of  its  action  as  a  mechanical 
pump).  Giddiness,  fainting,  cough,  shortness  of  breath, 
dropsy,  dyspepsia,  drowsiness,  etc.,  are  examples  of  this 
group,  to  which  the  term  '  mechanicar  may  be  appHed. 


64  Diseases  of  tJie  Heart. 

The  mechanical  symptoms  arc,  for  the  most  part,  due  to 
one  or  other  of  two  conditions,  viz. : — 

(a)  Defective  siipply  of  arterial  blood  to  distant  organs  and 
parts. — The  attacks  of  giddiness,  fainting,  the  feeble  motor 
power  in  the  lower  extremities,  and  the  muscular  twitchings 
in  the  face  and  lower  limbs,  which  are  seen  in  some  cases  of 
aortic  regurgitation,  are  good  examples  of  this  group  of 
symptoms. 

(b)  Venous  engorgeinent  of  distant  organs  and  parts. — 
The  symptoms  which  are  due  to  this  cause  are  both 
numerous  and  important.  In  fact,  many  of  the  most  pro- 
minent symptoms  in  cardiac  cases  are  due  to  the  secondary 
alterations  in  distant  organs,  and  to  the  complications  which 
result  from  the  long-continued  venous  engorgements  which  I 
am  now  describing.  Venous  engorgement  of  the  lungs,  for 
example,  produces  shortness  of  breath,  cough,  haemoptysis, 
etc.,  and  predisposes  to  the  attacks  of  bronchitis  and  pneu- 
monia, which  are  so  common  in  cardiac  cases,  and  which  are 
attended  by  characteristic  symptoms.  Venous  engorgement  of 
the  kidneys  produces  marked  alterations  in  the  urinary  secre- 
tion ;  the  amount  of  urine  is  diminished ;  the  specific  gravity 
is  high ;  the  urine  is  highly  coloured,  loaded  with  urates,  and 
often  albuminous.  In  the  course  of  time  a  form  of  cirrhosis 
of  the  kidney  may  be  established. 

In  addition  to  these  lung  and  kidney  symptoms,  others, 
due  to  engorgement  of  the  liver,  stomach,  intestines,  brain,  etc., 
are  commonly  observed  ;  while  the  congestion  of  the  subcutaneous 
veins,  and  the  veins  in  the  zualls  of  the  scrolls  cavities,  produces 
dropsy,  which  is  almost  invariably  first  observed  in  the  feet, 
but  which  may  ultimately  involve  an  extensive  area  of  the 
subcutaneous  cellular  tissue  and  almost  all  the  serous  cavities 
of  the  body.^  It  is  of  great  importance  to  remember  that  the 
occurrence  of  dropsy  in  these   cardiac  cases,  depends  in  no 


'  Cardiac  dropsy  begins  in  the  lower  extremities,  because  being  farther  removed 
from  the  heart,  the  circulation  in  them  is  slower  than  in  other  parts  of  the  body. 
It  is  generally  worse  at  night,  because  during  the  day,  when  the  patient  is  standing 
and  going  about,  the  return  current  of  blood  has  to  overcome  the  force  of  gravity 
in  its  passage  backwards  to  the  heart. 


Symptoms .  65 

small  degree  upon  the  condition  of  the  vaso-motor  nerve 
tone,  and  the  general  vitality — the  resisting  power,  so  to 
speak,  of  the  tissues.  The  composition  of  the  blood,  too,  is 
an  important  element  in  its  production. 

In  addition  to  the  two  great  groups  of  symptoms  already 
referred  to,  two  minor  groups  may  also  be  described  : — 

(a)  In  this  group  the  symptoms  are  for  the  most  part 
mechanical,  but  inasmuch  as  they  are  irregular  and  accidental 
in  their  occurrence,  should  be  distinguished  from  the  mechani- 
cal symptoms  which  I  have  hitherto  described.  To  these 
symptoms,  which  are  due  to  plugging  of  distant  vessels  by 
particles  of  fibrine  (emboli)  detached  from  clots  in  the  heart, 
or  from  vegetations  on  the  cardiac  valves,  the  term  accidental 
may  be  given. 

The  exact  nature  of  these  accidental  symptoms  depends 
for  the  most  part  upon  the  vessel  which  happens  to  be  ob- 
structed, upon  the  size  of  the  plug,  and  upon  the  rapidity 
with  which  the  obstruction  is  produced. 

Particles  of  fibrine  detached  from  the  cavities  or  valves 
of  the  right  heart  produce  embolic  infarctions  in  the  lungs, 
of  which  the  chief  symptom  is  haemoptysis  ;  limited  inflam- 
mation of  the  pleura  usually  results,  and,  in  those  cases  in 
which  the  infarction  is  of  large  size,  the  consolidation  of  the 
lung  which  it  produces,  can  be  recognised  by  percussion. 
Sudden  obstruction  of  the  main  branches  of  the  pulmonary 
artery — a  condition  which  seldom  occurs  in  cardiac  cases,  but 
which  is  sometimes  seen  after  delivery,  and  in  phlebitis, — may 
be  followed  by  immediate  death.  In  other  cases,  the  termina- 
tion is  not  so  rapid,  death  being  preceded  by  intense  dyspnoea, 
cyanosis,  quick  and  tumultuous  action  of  the  heart,  rapid 
elevation  of  temperature,  etc. 

When  the  embolon  is  detached  from  the  left  cavities,  it 
finds  its  way  into  some  of  the  branches  of  the  systemic  arterial 
circulation.  In  some  cases,  it  passes  up  the  left  common 
carotid  artery,  and  lodges  in  the  middle  cerebral  artery  of  the 
left  side,  producing  right-sided  hemiplegia  and  aphasia.  In 
some  of  these  cases  the  attack  is  ushered  in  by  sudden  loss 

E 


66  Diseases  of  the  Heart. 

of  consciousness,  in  others  there  are  epileptiform  convul- 
sions ;  in  others  again  (and  more  particularly  in  those  in 
which  the  hemiplegia  occurs  more  gradually)  consciousness  is 
retained. 

In  some  cases  the  embolon  lodges  in  the  spleen  ;  in 
others  in  the  kidney  ;  and,  in  fact,  it  may  be  carried  to  almost 
any  part  of  the.  body. 

The  pathological  character  of  the  plug  is  also  a  point 
of  some  importance.  In  ordinary  cases  it  consists,  as  I 
have  already  mentioned,  of  fibrine,  and  the  effects  which 
it  produces  are,  for  the  most  part,  mechanical.  In  many 
cases  of  ulcerative  endocarditis,  micrococci  abound  in  the 
vegetations  covering  the  affected  valves,  and,  being  conveyed 
by  the  emboli  to  distant  organs,  there  set  up  a  similar 
infective  process  to  that  which  is  occurring  in  the  heart. 

(b)  In  this  group  the  symptoms  are  the  result  of  pressure. 
In  intra-thoracic  aneurisms,  and  in  some  cases  of  pericarditis, 
for  instance,  prominent  symptoms,  such  as  pain,  dysphagia, 
alterations  in  the  voice,  cough,  etc.,  may  be  due  to  this  cause. 

The  more  particular  description  of  the  symptoms,  included 
in  these  four  groups,  will  be  more  appropriately  deferred  until 
I  come  to  treat  of  the  individual  cardiac  diseases  in  detail. 
But  it  may  perhaps  be  well,  before  going  further,  to  consider  a 
little  more  fully  than  we  have  yet  done,  dyspnoea,  cough,  and 
expectoration,  three  symptoms  which  are  very  common  in 
cardiac  cases,  and  which  may  be  due  to  a  considerable  variety 
of  different  conditions. 

Dyspncea. 

Alterations  of  the  breathing  are  frequently  met  with  in 
cardiac  and  arterial  disease.  In  some  cases,  the  difficulty 
of  breathing  is  only  occasional,  in  others,  it  is  constantly 
present ;  in  some  it  is  due  to  over-exertion  or  other  obvious 
exciting  cause  ;  in  others,  it  occurs  independently  of  any 
apparent  external  conditions.  The  chief  forms  of  dyspnoea, 
and  the  conditions  which  give  rise  to  them,  are  as  follows  : — 


Cardiac  Dyspncea.  67 

1.  Breathlessness  on  exertion  (going  up  stairs,  climbing  a 
hill,  etc.),  the  breathing  being  natural  when  the  patient  is  at 
perfect  rest.  This  is  the  most  common  form  of  cardiac  dys- 
pncea. It  occurs  more  particularly  in  mitral  lesions  ;  in  those 
cases  in  which  the  right  cavities  of  the  heart  are  dilated  ;  and 
in  cases  of  anaemia,  in  which,  as  we  have  seen,  cardiac  symp- 
toms are  common.  (The  dyspnoea  in  cases  of  anaemia  is 
doubtless  in  great  part  due  to  the  altered  composition  of  the 
blood  independently  of  the  cardiac  condition.) 

2.  The  dyspnoea  which  results  from  alterations  in  position 
(probably  from  alterations  in  the  position  of  the  diaphragm) 
independently  of  pulmonary  complications,  such  as  bronchitis, 
oedema  of  the  lungs  and  hydro-thorax.  In  many  cases  of 
advanced  cardiac  disease,  more  especially  when  the  aortic 
arch,  or  the  right  cavities  of  the  heart  are  much  dilated, 
dyspnoea  is  readily  excited  by  slight  changes  in  position.  It 
is  common  to  find  patients,  breathing  comfortably  and  quietly 
so  long  as  they  are  sitting  and  at  rest,  unable  to  lie  down  for 
some  time  after  getting  into  bed,  on  account  of  the  dyspncea 
produced  by  the  alteration  in  their  position.  In  some  cases 
the  heart,  after  a  time,  accommodates  itself  to  the  altered 
condition  of  things  ;  the  breathing  quiets  down,  and  the 
patient  falls  asleep. 

This  form  of  dyspnoea  is  probably  in  many  cases  due  to 
the  altered  position  of  the  diaphragm,  and  seems  closely 
allied  to  the  difficulty  in  breathing,  which  cardiac  patients 
so  frequently  experience  after  a  full  m.eal,  when  the  stomach 
becomes  distended  with  flatus,  during  attacks  of  dyspepsia, 
etc.  In  some  cases  it  seems  to  be  produced  by  reflex  im- 
pressions passing  from  the  stomach  through  the  vagus  nerve 
to  the  heart. 

3.  Paroxysmal  attacks  of  dyspnoea.  Sudden  difficulty 
in  breathing  is  occasionally  met  with  in  the  course  of 
cardiac  affections.  In  some  cases  it  is  due  to  sudden  over- 
distention  of  the  cardiac  cavities  ;  in  others,  to  spasm  of 
the  glottis,  produced  by  the  pressure  of  an  aneurism  of 
the  aortic  arch  upon  the  left  recurrent  laryngeal  nerve  ;  in 
others,    to    the    sudden    pressure    of  an    aneurism    upon    the 


68  Diseases  of  the  Heart. 

trachea  ;  in  others,  to  the  sudden  oedema  of  the  lungs, 
which  sometimes,  though  rarely,  results  from  excessive 
over-distention  of  the  left  ventricle  ;  in  others  to  sudden 
distention  of  the  right  ventricle,  and  imperfect  supply 
of  blood  to  the  lungs  ;  while  in  exceptional  cases  severe 
dyspnoea  may  be  caused  by  embolic  plugging  of  the  pul- 
monary artery. 

In  cases  of  this  description  the  difficulty  of  breathing  is 
intense;  the  patient  has  to  sit  up,  and  literally  to  fight  for 
breath.  The  duration  of  the  attack  varies  ;  in  some  cases,  it 
is  onl>'  temporary  ;  in  others  (as  for  instance,  in  the  case  of 
an  aneurism  pressing  upon  the  trachea  or  primary  bronchi) 
it  may  continue  for  several  days.  In  many  cases  death 
terminates  the  attack. 

4.  Typical  Orthopnoea.  In  other  cases  the  difficulty  in 
breathing  which  was  first  slight,  steadily  increases,  and  a 
permanent  condition  of  orthopnoea,  which  may  continue 
for  several  days,  or  even  weeks,  is  gradually  developed. 
Such  a  condition  is  common  in  the  late  stages  of  cardiac 
cases,  more  particularly  in  advanced  stages  of  mitral  disease 
and  in  dilated  conditions  of  the  right  heart.  The  patient  is 
more  or  less  cyanotic.  Dropsy  is  usually  a  prominent 
symptom,  and  the  difficult}'  in  breathing  depends,  in  many 
cases,  upon  pulmonary  complications,  such  as  hydro-thorax, 
bronchitis,  oedema  of  the  lungs,  etc. 

5.  Cheyne-Stokes'  Respiration  :  Angina  sine  dolore. — In 
some  cases  of  cardiac  disease,  more  particularly  where  the 
right  heart  is  dilated  and  fatt}-,  a  peculiar  form  of  rhythmical 
dyspnoea  is  observ^ed,  to  which  the  term  Cheyne-Stokes' 
respiration  is  given,  after  the  two  physicians  (Drs  Cheyne 
and  Stokes)  who  first  described  it.  In  this  form  of  dyspnoea 
the  patient  experiences  considerable  difficulty  of  breathing  for 
a  few  respirations.  The  dyspnoea  gradually  subsides,  the 
respirations  becoming  shallower  and  shallower,  slower  and 
slower,  until  for  a  time — it  may  be  for  half  or  three  quarters 
of  a  minute — they  are  entirely  suspended  ;  they  then  gradually 
reappear,  and  become  deeper  and  deeper,  quicker  and  quicker, 
until   the  height   of  the   paroxysm   of   dyspnoea   is   reached. 


Cheyne-Stokes  Respiratio7i,  69 

(See  fig.  16.)  The  same  sequence  of  events  then  recurs. 
The  duration  of  the  whole  cycle  from  the  height  of  one 
paroxysm  of  dyspnoea  to  the  height  of  the  next  paroxysm, 
is  usually  from  one  to  two  minutes,  half,  or  less  than  half, 
being  occupied  by  the  period  of  non-respiration  or  rest. 


Fig.  16. — Diagraniniatic  representation  of  Cheyne-Stokes'  Respiration. 

Cheyne-Stokes'  respiration  is  not  pathognomonic  of  any 
single  condition ;  it  is  a  rare  phenomenon,  and  has  been 
observed  in  : — (a)  advanced  cases  of  cardiac  disease  (more 
especially,  as  I  have  already  mentioned,  in  a  dilated  and  fatty 
condition  of  the  right  heart,  atheroma  of  the  coronary  arteries, 
and  dilatation  of  the  aorta)  ;  (b)  certain  cerebral  affections 
(more  especially  lesions  in  the  neighbourhood  of  the  medulla 
oblongata)  ;  (c)  uraemia  ;  and  (d)  very  exceptionally  in  other 
conditions. 

Cheyne-Stokes'  respiration  is  a  very  grave  and  ominous 
symptom  ;  it  only  occurs  in  advanced  cases  of  cardiac  disease, 
and  is,  as  a  rule,  speedily  followed  by  death.  It  is  closely 
allied  to  the  condition  which  is  termed  angina  sine  dolore. 
In  many  cases  of  Cheyne-Stokes'  respiration  the  arterial 
tension  is  very  markedly  increased  ;  this  was  notably  so 
in  two  typical  cases  which  have  come  under  my  own 
observation.  In  some  cases  the  condition  continues  for 
many  hours,  it  may  be  for  several  days  ;  the  sufferings  of 
the  patient  (though  not  painful  in  the  common  acceptation  of 
the  term)  are  extreme  ;  he  becomes  much  exhausted,  and 
often  very  drowsy  and  sleepy.  No  sooner,  however,  does  he 
dose  off  to  sleep  than  he  wakes  with  a  horrid  dream  or  with  a 
start ;  and  the  waking  is  always  associated  with  the  period  of 
dyspnoea,  i.e.  it  always  occurs,  so  far  as  my  observation  goes 
at  the  height  of  the  paroxysm  of  dyspncea. 


70  Diseases  of  the  Heart. 

In  Cheyne-Stokes'  respiration,  then,  there  is  an  alternate 
condition  of  dyspncea  and  apnoea,  the  two  conditions  being 
separated  by  a  gradual  rise  and  fall  in  the  depth  and  fre- 
quency of  the  respirations. 

The  exact  cause  of  the  condition  is  not  definitely  known. 
Its  immediate  cause  is,  without  doubt,  perverted  action  of  the 
respiratory  centre  in  the  medulla  ;  and  in  order  to  understand 
the  manner  in  which  this  perverted  action  may  be  brought 
about,  I  must  now  briefly  describe  the  nervous  mechanism  of 
respiration.     It  seems  probable  : — 

(i.)  That  the  nerve  impulses,  which  throw  the  respiratory 
muscles  (the  muscles  of  inspiration  and  expiration)  into  action, 
are  discharged  from  a  centre  which  is  situated  in  the  medulla 
oblongata — the  so-called  respiratory  centre.  (Respiratory 
centres  are  also  situated  in  the  spinal  cord,  but  that  in  the 
medulla  oblongata  is  certainly  the  most  important,  and  seems 
to  initiate  the  process,  and  to  control  the  action  of  the  lower, 
i.e.  of  the  spinal  respiratory  centres.) 

(2.)  That  under  normal  circumstances  the  action  of  this 
centre  is  rhythmical  and  automatic.  (This  point  is  not  ab- 
.solutely  determined,  but  it  seems  probable  that  the  action  of 
the  respiratory  centre  in  the  medulla  is  automatic.) 

(3.)  That  although  the  action  of  this  centre  (the  respiratory 
centre)  is  automatic,  its  discharges  (both  as  regards  their  force 
and  frequency)  may  be  influenced  by  external  conditions 
{i.e.  conditions  outside  the  centre)  ;  and  that  amongst  these 
external  conditions  the  amount  of  oxygen  supplied  to  this 
centre  by  the  blood  is  certainly  the  chief. 

When  the  blood  contains  a  small  amount  of  oxygen  {i.e. 
when  it  is  highly  venous),  or  when  the  arterial  blood  supply 
to  the  centre  is  diminished  or  abolished,  its  nerve  discharges 
are  increased,  i.e.  the  force  and  (to  a  less  extent)  the  frequency 
of  the  respiratory  movements  arc  increased  ;  in  other  words, 
a  condition  of  d)\spncea  may  be  developed.  The  attacks  of 
dyspnoea  which  occur  in  some  cases  of  cirrhotic  Bright's  dis- 
ease are  probably  due  to  this  cause,  viz.,  to  a  diminished 
supply  of  arterial  (oxygenated)  blood  to  the  respiratory 
centre.      In   chronic    Bright's   disease   the   arterial    tension    is 


Cheyne-Stokes  Respiration.  71 

extremely  high,  in  consequence,  it  is  supposed,  of  a  spas- 
modic contraction  of  the  arterioles,  and  we  can  easily  suppose 
that  when  the  arterioles  are  tightly  contracted,  the  blood 
supply  to  the  respiratory  centre  in  the  medulla  may  be  so 
much  diminished  as  to  produce  a  condition  of  dyspnoea. 
This  form  of  dyspnoea  is  sometimes  called  renal  asthma,  the 
term  is,  however,  a  bad  one,  for  the  condition  differs  from  the 
dyspnoea  of  spasmodic  asthma  in  this  important  particular, 
that  there  is  no  obstruction  to  the  passage  of  air  into  and  out 
of  the  air  cells.  The  respirations  are  not  only  more  frequent, 
but  they  are  much  deeper  than  in  health — to  use  the  expres- 
sive words  of  my  friend  Dr  Wyllie,  a  patient  affected  with 
this  form  of  dyspnoea  '  looks  as  if  he  had  just  been  running  a 
mile  race.' 

When,  on  the  contrary,  the  blood  is  over  oxygenated,  the 
nerve  discharges  from  the  respiratory  centre  are  diminished  in 
force  and  frequency,  and  a  condition  of  apnoea  may  result. 

A  free  supply  of  arterial  blood  to  the  medulla,  therefore, 
produces  diminution  of  the  respiratory  movements,  while  a 
diminished  supply  of  arterial  blood,  or  a  venous  condition 
of  the  blood,  is  attended  with  the  opposite  result. 

The  phenomena  of  Cheyne-Stokes'  respiration  are  pro- 
bably to  be  explained  (in  part  at  least)  by  the  fact,  that 
periodical  variations  occur  in  the  amount  of  oxygen  supplied 
to  the  respiratory  centre  in  the  medulla. 

Various  theories  have  been  advanced  to  explain  the  manner  in 
which  Cheyne-Stokes'  respiration  is  produced.  None  of  them  are,  to  my 
mind,  perfectly  satisfactory.  The  best  known  are  those  of  Traube  and 
Filehne. 

Traiibc's  T/ieory. — Traube,  starting  with  the  idea  that  in  the  different 
clinical  conditions,  which  give  rise  to  Cheyne-Stokes'  respiration,  there  is 
a  diminished  supply  of  properly  arterialised  blood  to  the  respiratory 
centre,  supposed  : — 

(i)  That  in  consequence  of  the  deficient  supply  of  oxygen,  the  irrita- 
bility of  the  respiratory  centre  is  so  materially  lowered,  that  a  much 
larger  accumulation  than  usual  of  carbonic  acid  in  the  blood  is  required 
to  arouse  it  into  action. 


72  Diseases  of  the  Heart. 

(2)  That  in  order  to  provide  this  increased  quantity  of  carbonic  acid, 
the  intervals  between  the  different  respiratory  acts  are  necessarily  pro- 
longed, and  that  it  is  in  this  manner  that  the  stage  of  apnoea  is  produced. 

(3)  That  at  the  end  of  the  period  of  apnoea,  the  accumulation  of  car- 
bonic acid  in  the  blood  is  so  great,  that  the  respiratory  centre  is  aroused 
into  action  ;  that  the  stimulation  is  at  first  slow  and  imperfect,  but  that 
it  gradually  gains  in  intensity  and  strength  until  the  discharge,  which  is 
excited  by  it,  is  so  violent,  that  a  condition  of  dyspnoea  is  produced. 

(4)  That  in  consequence  of  the  increased  respiratory  efforts  the  blood 
becomes  oxygenated  ;  the  respiratoiy  centre  is  therefore  no  longer  stimu- 
lated, and  in  consequence  of  the  cessation  of  the  stimulation,  or  possibly 
of  the  fact  that  its  irritability  is  exhausted,  the  respiratory  centre  gradually 
ceases  to  discharge,  and  the  period  of  apncea  supervenes. 

Various  objections  may  be  urged  against  this  view,  but  the  main  one 
—and  it  seems  to  me  a  fatal  one— is  this,  that  a  diminished  supply  of 
properly  arterialised  blood  to  the  respiratory  centre  would  excite  it  to  dis- 
charge, rather  than  lower  its  irritability.  Venous  blood  stimulates  the 
respiratory  centre,  not  so  much  because  it  contains  an  excess  of  carbonic 
acid,  as  because  it  is  deficient  in  oxygen.  With  regard  to  this  point, 
Dr  M.  Foster  says,  '  There  can  in  fact  be  no  doubt  that  the  action  of 
deficiently  arterialised  blood  on  the  respiratory  centre,  as  manifested  in 
an  augmentation  of  the  respiratory  explosions,  is  due  primarily  to  a  want 
of  oxygen,  and  in  a  secondary  manner  only,  to  an  excess  of  carbonic 
acid.'^  , 

Dr  Saiisom's  Modijicatioit  of  Trauhe's  TIieo>y. — Ur  Sansom  agrees 
with  the  latter  part  of  Traube's  theory,  but  supposes  that  the  impaired 
irritability  of  the  respiratory  centre,  which  Traube  attributes  to  a  deficient 
supply  of  sufficiently  arterialised  blood,  is  of  a  paralytic  character,  and 
that  in  many  cases  it  is  due  to  the  direct  result  of  a  cerebral  lesion.  '  I 
consider,'  he  says,  '  that  the  initial  lesion  is  paresis  of  the  respiratory 
centre,  and  though  this  paresis  may  be  produced  by  reflex  ner\'e  influence, 
it  is  usually  a  direct  exhaustion  from  cerebral  causes  — once  initiated,  the 
explanation  of  the  phenomena  on  the  theory  of  Traube  is  complete.'^ 

With  this  opinion  I  cannot  entirely  agree.  It  is  difficult  to  see  how 
a  centre,  which  is  in  a  state  of  paresis  or  paralysis  (unless  we  include 
under  that  head  a  condition  of  irritable  weakness  such  as  I  believe  to 
be  at  the  root  of  the  matter)  can  be  excited  to  such  vigorous  action 
as  the  respiratory  centre  evidently  is  ;  and  it  is  difficult,  I  think,  to  explain 
by  this  theory  the  total  cessation  of  the  respiration  which  occurs  during 
the  stage  of  apncea.  I  differ  from  Dr  Sansom  in  thinking  that  the  irrita- 
bility  of  the  respiratory   centre   is  impaired.       It  seems  to    me    that   a 

'   A  Text  Book  of  Physiology,  3d  edition,  p.  340. 
-  Diagnosis  of  Diseases  of  the  Heart,  p.  39. 


Cheyne-Stokes  Respiration.  ']-}y 

condition  of  irritable  weakness,  in  which  it  is  more  irritable^  more  easily 
excited  to  discharge,  but  at  the  same  time  more  easily  exhausted  than  in 
health,  would  more  satisfactorily  account  for  the  phenomena.  But  to  this 
point  I  will  presently  return. 

Filelijie's  Theory. — Filehne  believes  that  the  vaso-motor  centre,  as  well 
as  the  respiratory  centre,  is  concerned  in  the  production  of  the  condition. 
He  supposes  : — 

(i)  That  at  the  end  of  the  period  of  apnoea  the  deficiency  of  oxygen 
and  the  excess  of  carbonic  acid  in  the  blood,  stimulate  the  vaso-motor 
centre  ;  and  that  in  consequence  of  this  stimulation,  the  arteries  through- 
out the  body  (including  of  course  the  cerebral  vessels)  are  thrown  into  a 
condition  of  contraction. 

(2)  That  in  consequence  of  the  diminished  supply  of  arterial  blood  to 
the  respiratory  centre,  which  results  from  this  arterial  contraction,  stim- 
ulation of  that  centre  (the  respiratory  centre)  occurs,  and  is  manifested 
externally  in  the  form  of  dyspnoea. 

(3)  That  in  consequence  of  the  excessive  respiratory  efforts,  the 
blood  becomes  quickly  arterialised,  the  stimulation  of  the  vaso-motor 
centre  is  thereby  removed  ;  the  tonic  contraction  of  the  arteries,  therefore, 
disappears,  and  the  respiratory  centre  is  again  supplied  with  arterial 
blood.  Its  discharges,  therefore,  become  less  and  less  powerful,  and 
finally,  when  the  arterial  spasm  is  completely  removed,  the  respiratory 
centre  is  so  freely  supplied  with  arterial  blood  that  it  no  longer  discharges, 
and  the  condition  of  apnoea  is  produced. 

After  the  apnoea  has  continued  for  a  longer  or  a  shorter  period,  the 
blood  again  becomes  venous,  the  vaso-motor  centre  is  again  stimulated,  the 
arteries  again  contract,  and  the  whole  sequence  of  events  is  repeated. 

This  view  at  first  sight  seems  very  plausible,  but  it  is  certainly  incom- 
plete, unless  we  suppose  that  there  is,  in  addition,  some  condition  present 
which  renders  the  discharges  from  the  respiratory  centre  more  easy  at 
one  period  of  the  cycle  {i.e.  during  the  period  of  dyspnoea)  and  more  diffi- 
cult at  the  other  period  of  the  cycle  {i.e.  during  the  period  of  apnoea)  than 
they  are  in  health.  It  fails,  I  think,  to  account  for  the  phenomena,  unless 
we  grant  that  some  primary  alteration  in  the  respiratory  centre,  such  as 
I  have  indicated,  is  present.  If  the  conditions  which  Filehne  suggests 
are  all  that  are  required,  would  not  Cheyne-Stokes'  respiration  be  of  more 
frequent  occurrence  than  it  is  ?  Would  we  not  expect  it  to  be  produced 
in  every  case  in  which  the  blood  is  imperfectly  aerated?  Again,  it 
fails,  I  think,  to  account  satisfactorily  for  the  apnoea.  There  are  surely 
circumstances  of  every  day  occurrence  in  which  the  medulla  is  quite  as 
freely  supplied  with  arterial  blood  as  it  is  in  cases  of  Cheyne-Stokes' 
respiration  during  the  period  of  apnoea,  i.e.  after  the  arterial  spasm  is 
relaxed  ;  and  if  Filehne's  theory  is  correct,  why  is  it  that  in  these  cases 
apncea  is  not  produced  .'' 


74  Diseases  of  the  Heart. 

I  am  disposed,  therefore,  to  think  with  Dr  Sansom,  that  something 
more  is  necessary,  and  that  there  must  be  some  alteration  of  the  respira- 
tory centre  itself,  in  addition  to  the  conditions  which  Filehne's  theory 
supplies.  A  state  of  irritable  weakness  would,  in  my  opinion,  account 
for  the  condition. 

The  respiratory  centre  in  the  medulla  oblongata  probably  consists  of 
two  parts— one  connected  with  inspiration  (the  inspiratory  centre),  the 
other,  with  expiration  (the  expiratory  centre).  Now,  according  to  Rosen- 
thal (quoted  by  Dr  M.  Foster),  the  inspiratory  centre  is  the  seat  of  two 
conflicting  forces,  one  tending  to  generate  inspiratory  impulses  (the  dis- 
charging portion  of  the  inspiratory  centre,  as  we  may  call  it),  and  the 
other  offering  resistance  to  the  generation  of  these  impulses  (the  restrain- 
ing or  inhibiting  portion  of  the  inspiratory  centre),  the  one  and  the  other 
alternately  gaining  the  victory,  and  thus  leading  to  a  rhythmical  dis- 
charge.i 

Further,  we  may  probably  with  truth  suppose  that  the  two  parts  of  the 
inspiratory  centre  are  differently  acted  upon  by  the  same  stimulus  ; 
venous  blood,  for  instance,  which  excites  the  action  of  the  discharging 
portion,  depresses  the  action  of  the  restraining  portion,  vice  versa  arterial 
blood  depresses  the  action  of  the  discharging  portion,  but  strengthens 
the  action  of  the  restraining  part. 

Now,  if  we  suppose  that  the  discharging  portion  is  in  a  condition  of 
irritable  weakness,  in  which  it  is  more  easily  excited  to  discharge,  but  in 
which  it  tends  to  become  more  speedily  and  more  completely  exhausted 
than  in  health — (or,  better  still  perhaps,  that  both  portions  of  the  centre 
are  in  this  abnormal  condition,  i.e.  a  state  of  irritable  weakness),  we  have, 
I  conceive,  a  condition  of  things  which  will  satisfactorily  explain  the 
phenomena. 

Let  us  suppose,  as  it  is  simpler,  a  case  in  vvhich  the  discharging 
portion  is  in  a  condition  of  irritable  weakness,  the  restraining  portion 
remaining  normal.  Starting,  as  we  did  in  considering  Filehne's  theory, 
with  the  end  of  the  period  of  apnoea,  i.e.  with  the  blood  in  a  highly  venous 
condition  (see  fig.  17),  we  may  suppose  : — 

(l.)  That  the  venous  blood  gradually  excites  a  paroxysm  of  dyspnoea  : 
— Firstly  and  chiefl)'  by  acting  directly  upon  the  inspiratory  centre  itself, 
depressing  the  action  of  the  restraining  portion,  and  arousing  the  action 
of  the  discharging  portion,  which  has,  during  the  stage  of  rest  or 
apnoea,  been  graduall)-  recovering  from  the  condition  of  exhaustion 
occasioned  by  the  excessive  discharge,  which  produced  the  preced- 
ing paroxysm  of  dyspnoea.  Secondly.,  by  stimulating  the  action  of  the 
vaso-motor  centre,  in  consequence  of  which  the  arterioles  are  con- 
tracted, and  the  supply  of  oxygen  to  the  respiratory  centre  is  still  further 
diminished.     (See  fig.  18.) 

'    Text  Rook  of  Physiology^  3d  edition,  p.  336. 


Cheyne-Stokcs  Respiration.  75 

(2.)  That  in  consequence  of  the  excessive  ifritability  of  the  discharging 
portion  of  the  inspiratory  centre,  the  discharges  become  excessive,  and  a 
condition  of  dyspnoea  is  produced.     (See  fig.  19.) 

(3.)  That  in  consequence  of  the  iveakncss  of  the  discharging  portion  of 
the  inspiratory  centre  it  speedily  becomes  exhausted— over  exhausted  ; 
and  the  dyspnoea  tends  to  subside.     (See  fig.  20.) 

(4.)  That  in  consequence  of  the  excessive  respiratory  efforts  during 
the  paroxysm  of  dyspnoea,  the  blood  (which  was  previously  venous)  be- 
comes arterialised  ;  stimulation  of  the  discharging  portion  of  the  inspira- 
tory centre  ceases  ;  stimulation  of  the  restraining  portion  is  produced  ; 
and  in  consequence  of  the  deficient  stimulation  and  over-exhaustion  of 
the  discharging  portion,  the  restraining  portion  has  full  swing,  and  the 
condition  of  apnoea  is  produced.     (See  figs.  21  and  22.) 

The  arterialised  blood  acts  firstly  and  chiefly  upon  the  inspiratory- 
centre  itself,  strengthening  the  action  of  the  restraining  portion  and  de- 
pressing the  action  (removing  the  stimulation)  of  the  discharging  portion  ; 
secondly^  by  removing  the  stimulation  of  the  vaso-motor  centre,  in  conse- 
sequence  of  which  the  arterioles  dilate,  and  the  supply  of  oxygen  (arterial 
blood)  to  the  respiratory  centre  is  still  further  increased. 

During  the  stage  of  apnoea,  the  discharging  portion,  which  was  ex- 
hausted by  excessive  action  during  the  period  of  dyspnoea,  gradually 
regains  its  irritability,  and  the  condition  required  for  its  stimulation,  and 
for  the  removal  of  the  control  of  the  restraining  portion,  viz.,  a  venous 
condition  of  the  blood,  is,  in  consequence  of  the  absence  of  the  respirator}- 
movements,  gradually  developed. 

In  figures  17,  18,  19,  20,  21,  and  22,  1  have  endeavoured  to  represent 
the  changes  which  I  suppose  occur  in  the  different  periods  of  the  Cheyne- 
Stokes'  cycle. 

By  this  theor)-  we  can,  1  think,  satisfactorily  explain  : — 

[a]  The  occurrence  not  only  of  diminished  respiratory  movements 
after  the  period  of  dyspnoea,  but  the  complete  arrest  of  respiration  which 
occurs  during  the  stage  of  apnoea — a  point  which  it  is  difficult  to  explain 
by  the  other  theories. 

{b)  The  remarkable  fact  that  the  respiratory  centre  is  at  one  moment 
violently  discharging,  and  at  the  next  in  a  state  of  absolute  quiescence. 

if)  That  the  dyspnoea  and  apnoea  follow  one  another  with  rhythmical 
regularity  ;  and  that  the  one  condition  gradually  passes  into  the  other,  and 
vice  versd. 

It  is  perhaps  impossible  in  the  present  state  of  our  knowledge  to  ofter 
a  decided  opinion  as  to  the  manner  in  which  the  irritable  weakness  of  the 
vaso-motor  centre,  which  I  have  supposed  is  present  in  cases  of  Cheyne- 
Stokes'  respiration,  is  produced.  A  deficient  supply  of  arterial  blood  is 
probably  in  many  cases  one  factor  which  aids  in  the  production  of  the 
condition.  We  know  that  in  conditions  of  profound  aneemia,  an  extreme 
condition  of  irritable  weakness  of  the  spinal  centres  ^in  which  the  muscular 


76 


Diseases  of  the  Heart. 


Fir,.   17. 


18. 


Fig.    17.  —  The  end  of  the  pei  iod  of  afmva. 

1.  The  discharging  portion  of  the  inspiratory  centre  is  inactive  but  quite 
recovered  from  its  previous  exhaustion^d". 

2.  The  restraining  portion  of  the  inspiratory  centre  (r)  is  still  in  excess  =  r+, 
but  exhausted. 

3.  The  lungs  (L)  are  inactive. 

4.  The  blood  (B)  is  venous=V+  ;  and  a  stimulus  is  passing  : — to  the  dis- 
charging portion  of  the  inspiratory  centre  (d")  ;  and  to  the  vaso-motor  centre 
(VMC) 

5.  The  vaso-motor  centre  is  not  acting. 

6.  The  peripheral  blood  vessels  (b)  are  dilated  ;  and  charged  with  venous 
blood  ;  and  in  consequence  of  the  absence  of  oxygen,  the  discharging  portion  of 
the  inspiratory  centre  is  being  stimulated. 


Fig.   18.  —  The  cointneiue)iient  of  the  period  of  dyspnoea. 

1.  The  discharging  portion  of  the  inspiratory  centre  is  beginning  to  act,  and 
has  quite  recovered  from  its  exhaustion=d"  +  . 

2.  The  restraining  portion  is  not  acting  and  is  exhausted  =  r. 

3.  The  lungs  (L)  are  moderately  distended =moderate  dyspncea. 

4.  The  blood  is  highly  venous  (V  +  ),  and  a  stimulus  is  passing  :— to  the  dis- 
charging portion  of  the  inspiratory  centre,  and  to  the  vaso-motor  centre. 

5.  The  vaso-motor  centre  is  acting,  the  peripheral  blood-vessels  are  moderately 
constricted,  and  charged  with  highly  venous  blood  ;  a  stimulus  is  consequently 
passing  to  the  discharging  portion  of  the  inspiratory  centre. 


Cheyne-Stokcs  Respiration. 


n 


FIG.     19.  FIG.    20. 

Fig.  19.  —  The  period  of  the  height  of  the  dyspncea. 

1.  The  discharging'  portion  of  the  inspiratory  centre  is  acting  very  powerfully. 

2.  The    restraining    portion    is    inactive,    but    beginning    to    recover  from    its 
exhaustion. 

3.  The  lungs  (L)  are  acting  very  powerfully. 

4.  The  blood  is  anterio-venous=AV  ;  and  not  stimulating  any  of  the  centres. 

5.  The  vaso-motor  centre  is  discharging   powerfully  in  consequence  of  the 
previous  stimulation. 

6.  The  peripheral  blood-vessels  are  markedly  contracted,  and  the  discharging 
portion  of  the  inspiratory  centre  is  being  stimulated  by  the  want  of  oxygen. 


Fig.  20.  —  The  end  of  the  period  of  dyspnoea. 

1.  The  discharging  portion  of  the  inspiratory  centre  is  acting  feebly,  and 
rapidly  becoming  exhausted. 

2.  The  restraining  portion  has  recovered  from  its  exhaustion,  but  is  not  yet 
acting=r". 

3.  The  lungs  are  acting  feebly. 

4.  The  blood  is  arterial^A,  and  a  stimulus  is  beginning  to  pass  to  the 
restraining  portion  of  the  inspiratory  centre. 

5.  The  vaso-motor  is  still  acting,  though  feebly. 

6.  The  peripheral  blood-vessels  are  moderately  dilated,  and  charged  with 
arterial  blood  ;  a  stimulus  is  consequently  passing  to  the  restraivuiig  portion  of  the 
inspiratory  centre 


78 


Diseases  of  the  Heart. 


Fig.   21.  —  The  period  of  the  conimencetnent  of  apiiwa. 

1.  The  discharging  portion  of  the  inspiratory  centre  is  inactive  and  exhaust- 
ed=d. 

2.  The  restraining  portion  is  acting,  and  has  quite  recovered  from  its  previous 
exhaustion. 

3.  The  lungs  are  inactive. 

4.  The  blood  is  highly  arterial  (A+),  and  a  stimulus  is  passing  to  the  restrain- 
ing portion  of  the  inspiratory  centre. 

5.  The  vaso-motor  centre  is  not  acting. 

6.  The  peripheral  blood-vessels  are  dilated,  and  in  consequence  of  the  free 
supply  of  arterial  blood  the  restraining  portion  of  the  inspiratory  centre  is  being 
stimulated. 


Fig.  22.  —  The  period  of  the  height  of  the  apnan. 

1.  The  discharging  portion  of  the  inspiratory  centre  is  inactive,  but  beginning 
to  recover  from  its  exhaustion=d'. 

2.  The  restraining  portion  of  the  inspiratory  centre  is  still  acting  powerful- 
ly =r"+. 

3.  The  lungs  are  inactive. 

4.  The  blood  is  anterio-venous  (AV),  and  not  stimulating  any  of  the  centres. 

5.  The  vaso-motor  centre  is  inactive. 

6.  The  peripheral  blood-vessels  are  widely  dilated,  and  charged  with  blood, 
which  is  partly  arterial  and  partly  venous,  and  which  stimulates  neither  portion  of 
the  inspiratory  centre. 


Cheyne-Stokes  Respiration.  79 

power  is  defective,  muscular  nutrition  impaired,  but  muscular  irritability 
both  to  direct  and  reflex  stimulation  notably  increased)  is  often  observed  ; 
and  in  many  cases  of  Cheyne-Stokes'  respiration,  the  arteries  are  tightly 
contracted,  the  face  is  pale,  and  the  supply  of  arterial  blood  to  the  nerve 
centres  is  deficient,  i.e.  a  condition  of  local  anaemia  is  present. 

It  is  difficult,  however,  to  suppose  that  a  deficient  supply  of  blood  to 
the  vaso-motor  and  respiratory  centres  is  (even  in  these  cases)  the  sole 
cause  of  the  condition.  And  in  those  cases  in  which  the  arterial  tension 
is  not  increased,  and  in  which  there  is  no  anaemia,  it  is  obvious  that  some 
other  condition  must  be  present. 

Theoretically  we  may  suppose  that  the  condition  (irritable  weakness 
of  the  respiratory  centre  in  the  medulla)  may  be  produced  b)-  : — 

(rt.)   Lesions  of  the  medulla  itself 

ib^  Impressions  passing  to  it  from  the  higher  nerve  centres. 

And,  if  these  conditions  occur,  we  can  satisfactorily  explain  the  mode 
of  production  of  those  cases  of  Cheyne-Stokes'  respiration  in  which  there 
are  nervous  lesions,  and  in  which  the  heart  is  healthy. 

if)  Impressions  passing  to  it  from  the  periphery,  more  particularly 
from  the  heart  and  respiratory  organs  through  the  vagi  and  superior 
laryngeal  nerves. 

That  the  respiratoiy  centre  is  powerfully  affected  through  these  chan- 
nels, the  passage  quoted  in  the  foot-note  from  Prof  M.  Foster  clearly 
shows  ;  and  it  is  not  difficult  to  conceive  that  in  conditions  of  disease, 
profound  modifications  of  the  respiratory  centre  may  in  this  manner  be 
produced,  more  especially  in  those  cases  in  which  the  right  ventricle  is 
affected,  and  the  supply  of  blood  to  the  lungs  interfered  with.  Possibly 
then,  a  combined  condition  of  defective  arterial  blood  supply  to  the 
respirator)'  centre,  such  as  is  produced  by  a  tonic  contraction  of  the 
minute  arteries,  together  with  some  abnormal  stimulation  through  the 
vagi  or  superior  laryngeal   nerves,^  such  as  we  have  supposed   may  be 

'  '  Among  the  afferent  impulses  which  affect  the  automatic  action  of  the  centre ' 
{i.e.  of  the  respiratory  centre)  says  Dr  Michael  Foster,  '  the  most  important  are 
those  which  ascend  along  the  vagi.  If  one  vagus  be  divided,  the  respiration 
becomes  slower  ;  if  both  be  divided,  it  becomes  very  slow,  the  pauses  between 
expiration  and  inspiration  being  excessively  prolonged.  The  character  of  the 
respiratory  movement  too  is  markedly  changed  ;  each  respiration  is  fuller  and 
deeper,  so  much  so  indeed  that,  according  to  some  observers,  what  is  lost  in  rate 
is  gained  in  extent,  the  amount  of  carbonic  acid  produced  and  oxygen  consumed 
in  a  given  period  remaining  after  division  of  the  nerves  about  the  same  as  when 
these  were  intact.  Without  insisting  too  much  on  the  exactness  of  this  compensa- 
tion, we  may  at  least  conclude  from  the  effects  of  section  of  the  vagi,  in  the  first 
place,  that  during  life  afferent  impulses  are  continually  ascending  the  vagi  and 
modifying  the  action  of  the  respiratory  centre,  and  in  the  second  place,  that  the 
modification  bears  chiefly  on  the  distribution  in  time  of  the  afferent  respiratory 
impulses,  and  not  so   much  on   the  amount   to  which   they  are  generated.     These 


8o  Diseases  of  tJie  Heart. 

produced  by  the  cardiac  lesion  (more  particularly  by  a  dilated  condition 
of  the  right  heart),  may  be  the  cause  of  the  Cheyne-Stokes'  respiration 
which  is  met  with  in  some  cardiac  cases. 

The  whole  subject  {i.e  Cheyne-Stokes'  respiration)  requires  further 
elucidation.  It  is  only  by  the  accurate  examination,  and  by  the  pubHca- 
tion  of  a  considerable  number  of  cases  that  we  can  hope  to  arrive  at  a 
satisfactory  conclusion  as  to  the  exact  nature  of  the  condition.  In  order 
to  facilitate  the  study  of  these  cases  I  have  drawn  up  the  following 
memorandum  showing  the  points  to  which  attention  should  be  particularly 
directed  in  the  clinical  examination. 

The  points  to  which  attention  is  to  be  directed  in  the  clinical  examination 
of  Cheyne-Stokes'  respiration. 

A.  Preliminary  /"^rc/x— Name — Age— Sex— Occupation— Address  — 
Date  of  Examination. 

B.  History. 

(i.)  Of  the  present  illness. — The  date  of  commencement ;  the  exact 
mode  of  commencement  ;  the  supposed  cause  of  the  attack  ;  the  character 
of  the  symptoms  ;  the  order  of  their  appearance  ;  and  the  treatment 
which  has  been  adopted,  up  to  the  date  of  the  observation. 

(2.)  The  health  history  prior  to  the  commencement  of  the  present 
attack. 

(3.)  The  family  histoiy  ;  especially  the  occurrence  of  disease  of  the 
heart  or  kidneys  ;  and  of  attacks  of  Cheyne-Stokes'  respiration  amongst 
near  relatives. 

C.  The  present  condition. 

(l.)  The  nature  of  the  primary  (main)  disease. 

(2.)  The  condition  :—{a)  of  the  heart  (which  should  be  carefully  and 
methodically    examined    in    accordance   with    the   plan    of  examination 

afferent  impulses  are  probably  started  in  the  lungs  by  the  condition  of  the  blood  in 
the  pulmonary  capillaries  acting  as  a  stimulus  to  the  peripheral  endings  of  the 
nerves,  though  possibly  the  altered  air  in  the  air  cells  may  also  act  as  a  stimulus  to 
the  nerve  endings.'  .  .  .  Again,  'if  the  central  end  of  the  superior  laryngeal 
branch  of  the  vagus  be  stimulated,  whether  the  main  trunk  of  the  nerve  be  severed 
or  not,  a  slowing  of  the  respiration  takes  place,  and  this  may,  by  proper  stimula- 
tion, be  carried  so  far  that  a  complete  standstill  of  respiration  in  the  phase  of  rest 
is  brought  about,  i.e.  the  respiratory  apparatus  remains  in  the  condition  which 
obtains  at  the  close  of  an  ordinary  expiration,  the  diaphragm  being  completely 
relaxed.  In  other  words,  the  superior  laryngeal  nerve  contains  fibres,  the  stimula- 
tion of  which  produces  afferent  impulses,  whose  effect  is  to  inhibit  the  action  of  the 
respiratory  centre  ;  while  the  main  trunk  of  the  vagus  contains  fibres,  the  stimula- 
tion of  which  produces  afferent  impulses,  whose  effect  is  to  accelerate  or  augment 
the  action  of  the  respiratory  centre.' — A  Text -Book  of  Physiology,  io\\x\\\  edition, 
PP-  356,  357- 


Cough  and  Expectoration.  8i 

previously  described,  see  page  58)  ;  (i^)  of  the  lungs  ;  {c)  of  the  kidneys 
(amount  of  urine  in  twenty-four  hours,  its  colour,  reaction,  specific 
gravity,  presence  or  absence  of  albumen  and  casts)  ;  {d)  of  the  nerve 
centres. 

(3.)  The  appearance  of  the  patient  during  the  attack  of  Cheyne-Stokes' 
respiration,  and  the  sensations  which  he  experiences. 

(4.)  The  exact  character  of  the  respiration  itself.  The  exact  duration 
of  the  whole  cycle  ;  the  exact  duration  of  the  period  of  dyspnoea  ;  the 
number  and  character  (depth,  etc.)  of  the  respirations  during  the  period  of 
dyspnoea  ;  and  the  exact  duration  of  the  period  of  apnoea.  The  observer 
should  endeavour  to  represent  diagrammatically  on  paper  the  character 
of  the  respirations  during  the  whole  cycle  ;  preserving,  so  far  as  possible, 
the  relative  frequency  and  depth  of  the  respiratory  movements. 

(5.)  The  condition  of  the  peripheral  circulation.  The  colour  of  the 
face,  during  the  periods  of  dyspnoea  and  apnoea,  respectively.  The  fre- 
quency of  the  pulse  during  the  periods  of  dyspnoea  and  apnoea.  The  ten- 
sion of  the  pulse  during  the  periods  of  dyspnoea  and  apnoea.  In  all  cases 
sphygmographic  tracings  should  be  carefully  taken  both  during  the 
periods  of  dyspnoea  and  apncea,  and,  if  possible,  a  continuous  tracing 
during  the  whole  cycle,  i.e.  from  the  commencement  of  one  period  of 
dyspnoea  to  the  commencement  of  another  period  of  dyspnoea  should  be 
obtained. 

(6.)  The  treatment  adopted  and  its  effects  ;  in  particular,  the  effect  of 
nitrite  of  amyl  inhalations,  or  of  nitro-glycerine. 

(7.)  The  result. 

(8.)  In  fatal  cases  the  record  of  the /^'^Z-wfA'/tv;/ examination. 

Cough  and  Expectoration. 

Cough  is  a  common  symptom  in  cases  of  cardiac  disease. 
It  generally  depends  upon  venous  engorgement  of  the  lungs 
or  upon  the  secondary  pulmonary  complications,  such  as 
bronchitis,  oedema  of  the  lungs,  pneumonia,  etc.,  which  are,  as 
we  have  already  seen,  of  very  frequent  occurrence.  In  cases 
ot  this  description,  the  cough  is  usually  moist,  the  character 
of  the  expectoration  varying  with  the  nature  of  the  pulmo- 
nary complication.  In  other  cases,  the  cough  is  due  to  reflex 
irritation,  it  is  then  usually  dry,  and  often  has  a  harsh, 
brassy,  clanging  character.  Aneurisms  or  simple  dilatations 
of  the  aortic  arch,  which  exert  irritative  pressure  upon  the 
recurrent  laryngeal  nerve,  are  attended  by  a  characteristic 
cough  of  this  description.     A  short,  dry  cough  is  also  seen  in 

F 


82  Diseases  of  tJie  Heart. 

some  cardiac  cases  (in  which  there  are  no  distinct  pulmonary 
compHcations,  and  in  which  there  is  no  pressure  upon  the 
recurrent  laryngeal  nerve),  and  is  possibly  produced  by  reflex 
irritation  of  the  terminal  branches  of  the  cardiac  nerves  in  the 
walls  of  the  heart  itself. 

Expectoration. 

The  character  of  the  expectoration  depends  chiefly  upon 
the  exact  nature  of  the  pulmonary  complication  which  is 
present.  In  acute  bronchitis,  for  example,  the  expectorated 
matters  are  white  and  frothy,  and  consist  chiefly  of  water}- 
mucus  ;  in  chronic  bronchitis  the  expectoration  is  muco- 
purulent or  purulent ;  in  pneumonia  it  is  scanty  and  viscid, 
and  may  present  the  characteristic  rusty-red  colour  ;  in  very 
acute  cedema  of  the  lungs,  a  large  quantity  of  liquid  is 
suddenly  poured  out  into  the  air-cells  and  minute  bronchi, 
there  is  great  dyspnoea,  both  inspiration  and  expiration  may 
be  attended  with  a  loud  roaring  stridor,  and  the  patient 
may  expectorate  a  large  quantity  of  frothy  fluid,  which  in 
some  cases  is  highly  albuminous.  Haemoptysis  is  not  unfre- 
quent  in  the  course  of  cardiac  cases.  In  some  it  depends 
upon  simple  engorgement  of  the  lungs,  and  the  rupture 
of  dilated  capillaries  in  the  walls  of  the  air  cells.  In  this 
form  of  haemoptysis,  which  is  common  in  mitral  stenosis, 
the  blood  may  be  expectorated  in  considerable  quantities, 
and  is  often  quite  pure.  In  other  cases  haemoptysis 
depends  upon  embolic  plugging  of  some  of  the  pulmonary 
vessels  (pulmonary  infarctions) ;  in  cases  of  this  description 
the  blood  (which  may  at  first  be  pure)  soon  becomes 
of  a  dark  colour,  and  is  usually  mixed  with  considerable 
quantities  of  mucus  ;  as  the  case  progresses,  the  expectora- 
tion may  assume  various  shades,  and  may  become  foetid.  In 
other  cases  again,  haemoptysis  depends  upon  the  rupture 
of  an  aneurism  into  the  air  passages.  In  cases  of  this 
description,  the  blood  is  bright  and  florid,  and  the  bleed- 
ing may  be  sufficiently  copious  to  be  followed  by  immediate 
death. 


Comparative  value  of  di^ event  symptoms.  83 

T/ie  comparative  significance  of  '  subjective  cardiac  sensations,' 
and  of  symptoms  indicative  of  mechanical  derangement  oj 
the  circ2ilation. 

In  many  cases  of  functional  derangement  of  the  heart, 
more  especially  in  the  great  group  of  neurotic  lesions,  there 
are  no  '  mechanical '  symptoms,  but  the  patient  complains 
only  of  '  subjective  cardiac  sensations.'  He  often,  too,  is  im- 
pressed with  the  belief  that  he  has  heart  disease,  and  comes 
to  the  physician  with  the  express  object  of  having  his  heart 
examined. 

Persons  suffering  from  organic  cardiac  disease,  on  the 
contrary,  iisiially  complain  of  the  lung,  stomach,  and  other 
symptoms,  which  result  from  mechanical  derangement  of  the 
circulation,  though  they  may  in  addition  experience  and  com- 
plain of  '  subjective  cardiac  sensations.'  The  practical  lesson 
to  be  derived  from  these  facts  is,  that  persons  who  come  to  a 
physician  complaining  of  their  hearts,  and  zvho  do  not  manifest 
any  mechanical  disturbance  of  the  circulation,  are  in  all  pro- 
bability free  from  serious  cardiac  disease ;  ^  while  in  those 
cardiac  cases  in  which  such  symptoms  as  cough,  shortness  of 
breath,  dropsy,  etc.,  are  present,  as  the  result  of  the  cardiac 
lesion,  there  is  some  structural  alteration  which  has  produced 
mechanical  derangement  of  the  circulation  ;  occasionally,  as 
in  anaemia,  this  structural  alteration  is  temporary  and  curable, 
but  in  most  cases  it  is  permanent  and  '  organic'  The  reader 
must  not,  of  course,  conclude  from  this  statement,  that  the 
converse  proposition  holds  good,  viz.,  that  all  persons  who 
have  an  organic  cardiac  lesion,  manifest  well-marked 
symptoms.  Such  is  not  the  case,  for,  as  we  have  previously 
seen,  many  serious  organic  lesions  are  for  a  long  time  latent 
{i.e.  are  unattended  by  symptoms),  being  balanced  by  the 
compensatory  changes  which  occur. 

'  True  angina  pectoris  is  a  notable  exception  to  this  statement.  In  that  con- 
dition intense  pain,  commencing  in  the  region  of  the  heart,  and  radiating  up  to  the 
left  shoulder  and  down  the  left  arm,  is  experienced.  The  pain  is  attended  with  a 
dread  of  impending  death,  but  there  are  often  no  other  symptoms  indicative  of 
serious  organic  disease. 


84  Diseases  of  the  Heart. 

The  History  of  the  Case. 

History  of  the  present  illness. — In  the  first  place,  it  is  im- 
portant, if  possible,  to  ascertain  the  exact  date  at  which  the 
symptoms,  for  which  the  patient  comes  under  observation,  com- 
menced. By  determining  this  point  we  can,  provided  that  he 
has  been  previously  healthy,  ascertain  with  considerable  pro- 
bability whether  the  cardiac  lesion  is  a  recent  one  or  not.^ 

In  some  cases  the  point  is  easily  determined.  A  patient 
affected  with  aneurism,  for  example,  may  tell  you  that,  while 
making  some  violent  exertion,  he  felt  something  give  way 
in  the  chest  or  abdomen,  and  that  his  symptoms  date  from 
that  event.  In  cases  of  acute  rheumatic  inflammation  of  the 
heart,  there  is  usually  no  difficulty  in  fixing  the  exact  date  at 
which  the  rheumatic  attack  commenced.  So,  too,  in  some 
functional  derangements,  more  especially  in  some  forms  of 
neurotic  palpitation  and  the  like,  the  attack  comes  on  sud- 
denly and  abruptly,  the  patient  having  been  previously  free 
from  any  cardiac  symptoms.  But  in  other  cases,  more  espe- 
cially in  the  great  group  of  chronic  cardiac  affections,  the 
symptoms  develop  so  gradually,  and  the  case  progresses  so 
slowly,  that  the  patient  is  unable  to  fix  a  definite  date  for  the 
commencement  of  his  illness. 

In  the  second  place,  the  exact  mode  of  commencement  of  the 
attack,  the  character  of  the  symptoms,  and  the  manner  in  which 
they  are  progj'essing,  should  be  ascertained.  The  exact 
character  of  any  apparent  cause,  such  as  violent  effort,  mental 
agitation,  an  attack  of  rheumatism  or  scarlet  fever,  should 
be  carefully  investigated. 

In  the  third  place,  it  is  important  to  ascertain  the  nature 
of  the  treatment  %vhich  has  been  adopted  tip  to  the  time  ivhen  the 
patient  comes  under  observation.  Digitalis,  for  example,  when 
given  in  full  doses,  may  materially  modify  the  action  of  the 
heart  ;  the  knowledge,  therefore,  that  the  patient  had  been 
taking  large  doses    of  digitalis,    might  be    a    point    of  great 

The  fact  that  the  symptoms  are  of  recent  origin  is  not  proof  positive  that  the 
lesion  is  a  recent  one,  for  grave  cardiac  lesions  may,  as  I  have  repeatedly  pointed 
out,  he,  for  a  time  at  least,  unattended  by  any  obvious  symptoms. 


The  History  of  the  Case.  85 

practical  importance.  In  other  words,  the  nature  of  the  treat- 
ment which  has  been  previously  adopted,  may  give  us  a  clew- 
to  the  nature  of  the  case,  and  indicate  the  opinion  of  the 
previous  medical  attendant. 

The  history  of  the  state  of  health  before  the  commenceinent 
of  tlie  present  illness,  is  a  point  of  the  greatest  practical 
importance. 

The  patient  should  always  be  closely  questioned  as  to  the 
occurrence  of  previous  attacks  of  rheumatism,^  more  especially 
of  rheumatic  fever.  When  a  history  of  acute  rheumatism  is 
elicited,  it  is  important  to  ascertain  if  the  heart  was  affected 
during  the  attack.  The  fact  that  the  patient  was  leeched, 
cupped,  or  blistered  over  the  praecordia,  is  important  evidence 
in  those  cases  in  which  he  is  unable  to  give  us  any  definite 
information  on  this  point.  That  the  patient  has  been  short 
of  breath  on  exertion  (on  going  up  stairs,  up  a  hill,  etc.), 
since  the  attack  of  rheumatism,  is  also  highly  suggestive  of 
a  chronic  valvular  lesion,  although  he  may  have  in  other 
respects  enjoyed  good  health.  Scarlet  fever  is  another 
disease,  which  is,  not  unfrequcntly,  attended  with  endo- 
carditis ;  and  in  children,  who  come  under  treatment  for 
valvular  lesions,  it  is  important  (more  especially  where  there 
is  no  history  of  rheumatism)  to  inquire  into  this  point.  I 
might  mention  many  other  conditions  which  sow  the  seeds  of 
subsequent  cardiac  or  arterial  disease  (syphilis,  for  example, 
is  an  important  cause  of  aneurism),  they  will  however  be 
detailed  when  I  come  to  speak  of  the  aetiology  of  the  in- 
dividual cardiac  diseases. 

The  habits  and  mode  of  life,  and  general  surroundings  of 
the  patient,  are  of  great  importance,  more  especially  in  deter- 
mining the  plan  of  treatment :  but  these  points  will  be  more 
appropriately  considered  afterwards. 

'  It  is  important  to  remember  that  endocarditis  may  develop  in  the  course  of 
mild  and  apparently  insignificant  attacks  of  subacute  rheumatism.  Many  persons, 
too,  more  especially  in  the  lower  ranks  of  life,  do  not  appreciate  the  difference 
between  ordinary  muscular  rheumatism  and  rheumatic  fever  (articular  rheumatism.) 
It  is  well,  therefore,  in  the  first  instance  to  ask  the  patient  if  he  has  suffered  from 
rheumatism,  and  if  he  answer  in  the  affirmative,  to  question  him  as  to  the  e.xact 
nature  of  the  attack 


86  Diseases  of  the  Heart. 

Family  History. — Acute  rheumatism,  which  is  such  a  fertile 
source  of  cardiac  valvular  lesions,  is  much  more  frequent  in 
some  families  than  in  others  ;  and  it  is  in  consequence  of  their 
liability  to  rheumatism,  that  the  members  of  these  families 
are  more  apt  to  be  affected  with  cardiac  valvular  lesions  than 
other  people.  But,  independently  of  the  rheumatic  tendency, 
some  persons  inherit  ^a  tendency  to  disease  of  the  heart  and 
vascular  system.  For  example,  the  late  Dr  Charlton  of 
Newcastle-on-Tync,  told  me,  that  two  brothers,  in  easy 
circumstances,  who  had  not  been  exposed  to  any  undue  strain, 
and  who  had  not  suffered  from  rheumatism,  came  under  his 
care,  suffering  from  atheroma  of  the  thoracic  aorta,  and  died 
at  the  unusually  early  ages  (for  atheroma)  of  twenty-three 
and  twenty-five.  In  these  cases  it  was  difficult  to  resist  the 
conclusion  that  the  condition  was  hereditary.  In  later  life, 
when  arterial  degeneration  is  common,  this  hereditary  ten- 
dency to  atheroma  is  still  more  apparent.  In  some  cases 
it  seems  to  be  due  to  gout  ;  in  others  it  is  associated  with 
kidney  disease.  Those  functional  forms  of  cardiac  derange- 
ment, which  depend  upon  disordered  innervation  of  the  heart, 
are  more  common  in  persons  of  a  neurotic  temperament  than 
in  other  people  ;  and  as  we  all  know  the  neurotic  tempera- 
ment is  eminently  hereditary. 

PRESENT   CONDITION. 

[The  date  at  which  the  examination  is  made  should  be  stated,  for  in 
hospital  practice  several  days  may  elapse  between  the  admission  of  the 
patient  and  the  noting  of  the  case.] 

The  Physiognomy  of  the  Case. — While  the  preliminary 
facts  and  previous  history  are  being  investigated,  the  phy- 
sician is  both  consciously  and  unconsciously  learning  many 
important  particulars  as  to  the  nature  of  the  case. 

In  some  cases  the  physiognomy  not  only  suggests  the 
nature  of  the  lesion,  but  also  indicates  its  severity.  Attention 
must  be  particularly  directed  to  : — 

I.  The  colour  of  the  face  (of  the  lips,  nose,  and  ears  more 
especially,). 


1  he  Colour  of  the  Face.  87 

2.  The  presence  of  subcutaneous  dropsy  (in  the  feet,  face, 
and  hands  more  particularly.) 

3.  The  facial  expression. 

4.  The  condition  of  the  breathing. 

5.  The  attitude. 

6.  The  general  state  of  nutrition. 

The  Colour  of  the  Face. 

By  observing  the  colour  of  the  face  we  get  important 
evidence  as  to  the  condition  of  the  capillary  circulation  ;  and 
hence  as  to  the  manner  in  which  the  circulation  is  being  car- 
ried on — a  point  of  the  greatest  importance  in  cases  of  cardiac 
disease.  In  some  cases  the  colour  of  the  face  is  natural  ;  in 
others  it  is  more  dusky  than  in  health  ;  in  others,  again,  it  is 
paler  than  normal. 

Natural  Colour  of  the  Face. — In  many  functional  affections, 
more  particularly  the  neurotic  disorders  of  the  heart  ;  in 
many  aneurisms  ;  in  aortic  stenosis  ;  in  slight  cases  of  aortic 
regurgitation  ;  and  in  mitral  cases  (more  especially  mitral 
stenosis),  so  long  as  compensation  is  perfect,  the  colour  of  the 
face  may  be  quite  natural. 

Blucuess  of  the  face — Cyanosis. — Anything  which  inter- 
feres with  the  circulation  of  the  blood  in  the  lungs,  with  the 
passage  of  the  blood  through  the  right  cavities  of  the  heart, 
or  which  prevents  the  return  of  blood  to  the  heart,  such  as 
pressure  on  the  superior  cava,  will  produce  venous  congestion, 
and  hence  blueness  of  the  face.  The  cyanosis  is  most  marked 
in  those  cases  in  which  there  is  a  backwash  through  the  tri- 
cuspid, or  in  which  the  venous  and  arterial  blood  currents 
are  intermixed,  as  they  are  in  some  congenital  malformations. 

Congenital  Cyanosis,  in  which  the  blueness  is  often  extreme 
(hence  the  term  morbus  ceruleus,  which  has  been  given  to  these 
cases),  usually  depends  upon  some  cardiac  malformation,  such 
as  stenosis  of  the  orifice  of  the  pulmonary  artery  w^ith  a  patent 
condition  of  the  foraman  ovale,  or  upon  transposition  of  the 
aorta  and  pulmonary  artery  (the  aorta  arising  from  the  right, 
and  the  pulmonary  artery  from  the  left  ventricle). 

Acquired  Cyanosis. — When  the  cyanosis  is  extreme,  there 


88  Diseases  of  the  Heart. 

is  generally,  in  my  experience,  long  standing  disease  of  the 
lungs  or  disease  of  the  right  cavities  of  the  heart,  permitting 
of  tricuspid  regurgitation  :  the  two  conditions  being  generally 
combined.  Cases  are,  for  instance,  not  unfrequently  met  with 
in  which  there  is  a  history  of  repeated  attacks  of  bronchitis 
since  childhood  ;  in  which  the  patient  has  for  years  been  short 
of  breath  ;  in  which  the  lungs  are  emphysematous  or  cirrhotic  ; 
and  in  which  the  right  cavities  of  the  heart  are  hypertrophied 
and  dilated.  In  cases  of  this  description,  there  is  always  more 
or  less  blueness  of  the  lips,  and  any  increased  obstruction  to 
the  aeration  of  the  blood  in  the  lungs  (such  as  is  occasioned 
by  an  attack  of  acute  bronchitis,  pneumonia,  etc.),  or  any  in- 
creased distention  of  the  right  cavities  of  the  heart,  may  be 
attended  with  the  most  extreme  degree  of  cyanosis. 

In  mitral  cases  in  which,  as  we  have  previously  seen,  the 
free  circulation  through  the  lungs  is  interfered  with,  and  in 
which  secondary  changes  in  the  right  heart  are  so  commonly 
observed,  more  or  less  cyanosis  is  usually  present,  but  it  is 
seldom  so  great  as  in  the  cases  of  primary  pulmonary 
obstruction  to  which  I  have  just  alluded,  and  is  often  asso- 
ciated with  some  degree  of  ansemia.  While  compensation  is 
perfect  the  colour  of  the  face  may  be  quite  natural. 

In  all  of  these  cases,  but  less  so,  I  think,  in  congenital 
cyanosis  than  in  the  other  two,  the  face  may  be  somewhat 
swollen  as  well  as  cyanotic. 

When  the  return  current  of  blood  through  the  superior 
vena  cava  is  interfered  with,  as  it  is  sometimes  by  the  pressure 
of  an  aneurism  or  solid  intra-thoracic  growth,  the  lips,  ears, 
nose,  etc.,  are  more  or  less  livid.  In  these  cases  there  is 
marked  oedema,  which  is  not,  of  course,  confined  to  the  face, 
but  is  seen  in  all  the  parts  (face,  neck,  upper  extremities,  and 
upper  part  of  the  thoracic  parieties)  from  which  the  superior 
cava  draws  its  blood-supply.  In  consequence  of  the  oedema, 
the  face  in  the  region  of  the  eyelids,  etc.,  is  usually  pale,  and 
the  condition  may  at  first  sight  be  mistaken  for  a  case  of 
Bright's  disease.  The  marked  lividity  of  the  lips,  ears,  etc., 
and  the  limitation  of  the  swelling  to  the  area  of  distribution 
of  the  superior  cava,  at  once,  distinguish  the  two  conditions. 


Subcutaneous  Dropsy.  89 

Pallor  of  the  Face. — In  cases  of  free  aortic  regurgita- 
tion, in  which  the  arterial  system  is  imperfectly  distended 
during  the  diastole  of  the  ventricle,  the  face  is  pale, 
generally  thin,  and  there  is  often  an  anxious  expression  of 
countenance.^ 

In  conditions  of  aiiccinia,  in  which,  as  we  have  pre- 
viously seen,  cardiac  symptoms  and  cardiac  murmurs  are 
common,  the  face  and  mucous  membranes  are  unusually 
pale  ;  in  chlorosis  and  progressive  pernicious  ancsinia,  the  face 
may  be  slightly  puffy,  and  generally  has  a  lemon  yellow  hue, 
which  must  be  distinguished  from  the  dingy,  yellow  colour, 
which  is  seen  in  many  cases  of  advanced  mitral  disease.- 

Cardiac  lesions  are,  of  course,  frequently  met  with  in  con- 
nection with  Bright's  disease  ;  and  in  combined  cases  of 
cardiac  and  renal  disease,  the  pale,  puffy  face  which  is  charac- 
teristic of  the  large  white  kidney,  or  the  dingy  colour  of  the 
face  which  is  seen  in  the  cirrhotic  form  of  Bright's  disease, 
may,  of  course,  be  met  with. 

The  presence  oj  subcutaneous  dropsy. 

As  we  have  previously  seen,  dropsy  is  of  frequent  occur- 
rence in  advanced  cases  of  cardiac  disease  (more  especially 
mitral  and  right  sided  lesions)  ;  and  it  almost  invariably  com- 
mences in  the  feet.^     I  have  already  alluded  to  those  cases  of 

'  This  statement  does  not,  of  course,  apply  to  those  cases  oi  aortic  regurgitation 
in  which  the  mitral  valve  has  given  way.  In  combined  cases  of  this  description, 
more  particularly  when  the  mitral  regurgitation  is  free,  there  may  be  some  blueness 
of  the  lips. 

^  In  both  ot  these  cases  the  conjunctiva  may  be  yellow.  In  the  former  (chlo- 
rosis) the  yellow  colour  is  seen  chiefly  at  the  inner  and  outer  canthi,  and  is  due  to 
a  deposit  of  sub-conjunctival  fat ;  in  the  latter  (advanced  cases  of  mitral  disease, 
tricuspid  regurgitation,  etc.)  the  yello\v  discolouration  of  the  skin  is  of  a  darker, 
dingier  hue,  and  usually  depends  upon  congestion  of  the  liver. 

^  A  swollen  condition  of  the  feet,  untied  shoes,  slit-up  trousers,  etc.,  at  once 
suggest  a  cardiac  lesion.  The  same  form  of  dropsy  [i.e.  dropsy  beginning  in 
the  feet)  may  be  due  to  simple  debility,  to  anything  which  interferes  with  the 
return  current  through  the  inferior  vena  cava,  or  to  primary  obstruction  to  the 
blood  in  the  lungs,  such  as  is  produced  by  cirrhosis,  emphysema,  etc.  The 
differential  diagnosis  which  can  generally  be  made  without  much  difficulty,  will  be 
more  particularly  described  under  the  head  of  valvular  lesions. 


90  Diseases  of  the  Heart. 

local  dropsy  (dropsy  confined  to  the  face,  neck,  and  upper 
extremities)  due  to  the  pressure  of  an  aneurism  or  intra- 
thoracic growth  upon  the  superior  cava. 

The  Facial  Expression. 

The  facial  expression  (irrespective  of  the  colour  of  the 
face  and  the  presence  or  absence  of  oedema)  does  not,  as 
a  rule,  afford  much  information.  In  exophthalmic  goitre, 
in  which  cardiac  symptoms  and  signs  are  usually  prominent, 
the  projecting  eyeballs  at  once  attract  attention.  In  some 
cases  of  aortic  disease,  or  of  aneurism,  the  expression  may  be 
anxious  and  indicative  of  suffering.  During  the  paroxysm  of 
angina  pectoris,  in  conditions  of  orthopncea,  and  Cheyne- 
Stokes'  respiration,  an  expression  of  horror,  dread,  anguish,  or 
intense  suffering,  may  be  present.  In  advanced  conditions  of 
cyanosis,  in  which  the  cerebral  centres  are  imperfectly  sup- 
plied with  arterial  blood,  the  patient  is  often  drowsy  and  the 
expression  apathetic. 

The  Condition  of  the  Breathing. 

In  cases  of  aortic  disease  there  may  be  no  disturbance  of 
the  respiration.  In  other  cases  of  cardiac  disease,  one  or  other 
of  the  different  forms  of  dyspnoea,  which  I  have  previously 
described  (see  page  66),  may  be  present. 

T/ie  Attitude. 

In  acute  cases  the  patient  is  usually  in  bed,  not  so  much 
on  account  of  the  cardiac  complication  as  on  account  of  the 
primary  affection  (acute  rheumatism,  etc.) ;  he  usually  lies  on 
his  back,  and,  so  far  as  possible,  avoids  movement. 

In  those  cases  of  cardiac  disease,  both  acute  and  chronic, 
in  which  the  respiratory  functions  are  seriously  interfered 
with,  the  patient  is  unable  to  lie  down,  and  a  condition  of 
typical  orthopncea  may  be  present.  Frequently  he  will  not 
go  to  bed,  but  sits  up  in  a  chair  for  days  and  nights— it  may 
be  for  weeks— together.     The  position,   in    which    he  places 


The  General  State  of  Nutrition.  9 1 

himself  in  order  to  get  relief,  is  sometimes  a  striking  one  ; 
when  he  is  sitting  in  a  chair  or  on  the  side  of  the  bed,  the 
head  is  bent  forwards,  the  weight  of  the  trunk  being  supported 
by  the  arms,  which  are  kept  rigid,  the  hands  grasping  the 
thighs  just  above  the  knees  ;  in  this  position  the  parts  are  so 
fixed  that  the  respiratory  muscles,  more  particularly  the 
extraordinary  muscles  of  respiration,  are  able  to  act  with 
great  advantage  ;  in  other  cases,  he  leans  over  the  back  of  a 
chair,  or  kneels  on  the  floor,  resting  his  head  and  forearms  on 
the  bed,  or  sits  resting  them  on  a  table,  mantlepiece,  etc. 

Patients  suffering  from  aneurism  sometimes  assume 
peculiar  positions  in  order  to  remove  the  pressure  of  the  sac 
from  the  surrounding  parts  ;  in  some  cases  of  abdominal 
aneurism,  for  example,  the  patient  can  only  lie  on  his  face  ; 
in  others,  he  can  only  get  relief  from  paroxysms  of  pain  by 
resting  on  his  hands  and  knees  ;  in  others,  again,  the  thigh  is 
flexed  upon  the  abdomen.  But  more  minute  and  detailed 
description  of  the  various  attitudes  which  may  be  assumed  in 
individual  cases,  would  obviously  be  out  of  place  here. 

The  General  State  of  Nutrition. 

The  cardiac  affections  which  seriously  embarrass  the 
respiration,  and  cause  secondary  disturbances  in  the  liver, 
stomach,  and  other  abdominal  organs,  are  usually  attended 
with  very  considerable  derangement  of  the  nutritive  functions. 
In  mitral  cases,  for  example,  after  the  failure  of  compensation, 
the  patient  becomes  soft  and  flabby,  and  there  is  usually  con- 
siderable emaciation  ;  it  must  of  course  be  remembered  that 
when  the  subcutaneous  fat  is  abundant,  or  there  is  great 
dropsy,  the  emaciation  may  escape  detection  unless  carefully 
looked  for. 

In  aortic  cases  the  patient  is  usually  spare,  but  the  general 
state  of  nutrition  is,  as  a  rule,  fairly  well  preserved. 

In  some  cases  of  aneurism  there  is  no  impairment  of  the 
general  health  ;  indeed  one  of  the  most  striking  features  is 
often  the  total  want  of  proportion,  so  to  speak,  between  the 
severity  of  the  disease  and  the  general  constitutional  state. 


92  Diseases  of  the  Hcaj-t. 

THE   PHYSICAL   EXAMINATION    OF   THE   HEART   AND 
ORGANS   OF   CIRCULATION. 

The  object  of  the  physical  examination  of  the  heart  and 
organs  of  circulation  is,  of  course,  to  ascertain  their  exact 
physical  condition.  We  endeavour  to  determine  the  physical 
condition  of  the  heart  itself ;  of  the  great  blood-vessels  within 
the  thorax  and  abdomen  ;  and  the  manner  in  which  the  peri- 
pheral circulation  is  being  carried  on.  The  methods  of 
examination  which  we  chiefly^  employ  are  inspection,  pal- 
pation, percussion,  auscultation,  and  the  use  of  the  sphygmo- 
graph. 

THE   PHYSICAL   EXAMINATION    OF   THE   HEART. 

The  object  of  the  physical  examination  of  the  heart  is  to 
determine — 

1,  The  exact  frequency^  rhythm,  and  character  (whether 
slow  and  laboured,  quick  and  irritable,  etc.)  of  its  contrac- 
tions. 

These  points  are  determined  by  observing  the  character  of 
the  pulse  ;  by  inspecting  and  palpating  the  praecordia  ;  and 
by  auscultating  the  heart  ;  the  examination  of  the  pulse 
being  especially  valuable. 

2.  Its  position  in  the  thorax  ;  its  size  and  shape  as  a  luhole  ; 
and  the  relative  size  and  shape  of  its  component  parts. 

We  determine  these  points  chiefly  by  inspecting  the  prae- 
cordial  region  {i.e.  by  observing  by  means  of  inspection  the 
position,  extent,  and  character  of  the  visible  impulse);  by 
palpating  the  praecordial  region  {i.e.  by  observing  by  means 
of  palpation  the  position,  extent,  and  character  of  the 
visible  impulse) ;  and  by  percussing  the  praecordial  region 
{i.e.  by  determining  by  means  of  percussion  the  exact  extent, 
shape,  and  outline  of  the  cardiac  dulness). 

Percussion  is  particularly  valuable  in  determining  these 
points. 

'  The  cardiograph  is  not  yet  employed,  even  in  hospitals,  as  one  of  the 
ordinary  methods  of  examination  ;  it  is  not,  therefore,  described  in  the  text,  but  in 
the  appendix. 


The  Physical  Examination  of  the  Heaj't.  93 

3.  The  condition  of  its  valvular  apparatus. 

The  condition  of  the  valvular  apparatus  of  the  heart  is  chiefly 
determined  by  means  of  auscultation.  Palpation  in  some 
cases  also  affords  information.  The  exact  size  and  shape  of 
the  heart  and  of  its  component  cavities  (which  are,  as  we  have 
just  seen,  chiefly  determined  by  means  of  percussion),  cor- 
roborate the  information  derived  from  auscultation  ;  while 
very  important  evidence  as  to  the  condition  of  the  valvular 
mechanism,  is  also  obtained  by  observing  the  condition  of 
the  circulation  in  front  of  and  behind  the  valve  which  is  being 
examined.  The  mode  of  examination  will  afterwards  be 
described. 

4.  The  state  of  its  musciilar  zualls  (whether  hypertrophied, 
dilated,  degenerated,  etc.). 

We  determine  this  most  important  point  by  observing : — 
{a)  The  size  of  the  heart  and  of  its  component  parts  (in- 
spection, palpation,  and  percussion  of  the  prsecordia). 

f)  The  force  and  character  of  the  cardiac  impulse  (palpa- 
tion of  the  praecordia) ;  the  force  and  character  of  the  pulse ; 
the  loudness  and  other  characters  of  the  heart  sounds  (auscul- 
tation of  the  prsecordia),  and  the  condition  of  the  peripheral — 
arterial  and  venous — circulation.  Corroborative  evidence  is 
also  afforded  in  many  cases  by  observing  the  general  condition 
of  the  system,  and  the  state  of  particular  organs,  such  as  the 
lungs  and  kidney  :  profound  anaemia,  for  example,  suggests 
fatty  degeneration  of  the  heart  ;  kidney  disease  (especially 
cirrhosis),  hypertrophy  of  the  left  ventricle. 

5.  The  condition  of  the  pericardial  sac. 

This  point  is  chiefly  determined  by  means  of  auscultation 
and  percussion. 

INSPECTION    AS   APPLIED    TO    THE    EXAMINATION    OF   THE 
HEART  ;    INSPECTION    OF    THE    PR/ECORDIAL    REGION. 

By  the  praecordial  region  we  understand  that  part  of  the 
chest  wall  which  lies  in  front  of  the  heart.  It  is  necessary, 
therefore,  before  proceeding  further,  to  define  the  exact 
position  of  the  heart  in  the  thorax,  and  to  describe  the  limits 
of  the  praecordial  region. 


94  Diseases  of  the  Heart. 

The  position  of  the  Heart  in  the  Thorax. 

The  heart,  contained  in  the  fibro-serous  bag  termed  the 
pericardium,  is  placed  obHquely,  with  its  long  axis  from  right 
to  left,  in  the  lower  part  of  the  anterior  mediastinum  (see 
fig.  23).     It  consists  of  four  chambers,  two  auricles  and  two 


KiG.   23. — The  heart  and  great  vessels  in  situ.     ^  Enlarged  from  Sibson. ) 
The  lungs  have  been  drawn  aside,  and  the  anterior  surface  of  t-he  pericardial 
sac  removed. 


TJie  Position  of  tJie  Heart  in  tJie  TJiorax.         95 

ventricles  ;  and  in  the  adult  male,  after  death,  is  about  the 
size  of  the  closed  fist.  It  rests  upon  the  central  tendon  of 
the  diaphragm,  is  attached  above  by  its  base  to  the  great 
vessels,  and  is  almost  completely  surrounded  by  the  lungs, 
which,  with  the  bony  walls  of  the  chest,  protect  it  from 
external  injury. 

The  base  corresponds  to  the  junction  of  the  upper  margins 
of  the  third  costal  cartilages  ;  the  apex  to  the  5th  interspace, 
or  the  6th  rib.  (In  the  adult  male  the  apex-beat  can  usually 
be  felt  between  the  5th  and  6th  ribs,  at  a  point  about  an 
inch  and  a  half  below,  and  slightly  within  the  left  nipple.) 
As  a  zutiote,  then,  the  heart  extends  vertically  from  the  2nd 
interspace  above,  to  the  6th  rib  below  ;  and  transversely, 
from  a  little  within  the  left  nipple,  to  a  finger's  breadth  or 
more  to  the  right  of  the  sternum  ;  and  this  space  which 
the  heart  occupies,  as  a  whole,  is  called  the  deep  cardiac 
region. 

Nearly  two-thirds  of  the  organ  lie  to  the  left,  and  more 
than  one-third  to  the  right  of  the  middle  line.  Sibson  points 
out  that  when  the  left  lung  is  unusually  large,  i.e.  larger  than 
the  right,  the  heart  is  situated  more  to  the  right ;  and  vice 
versa,  when  the  right  lung  is  larger  than  normal  (irrespective, 
of  course,  of  any  disease,  for  we  are  now  considering  the 
position  in  health),  the  heart  may  be  situated  more  to  the 
left. 

The  relationship  of  the  Heart  to  the  surface  of  the  Chest. 

The  prsecordial  region  (that  part  of  the  chest  wall  which 
lies  in  frojit  of  the  heart)  includes,  therefore,  the  greater  part 
of  the  lower  sternal  and  left  mammary,  and  part  of  the  right 
mammary,  regions.     (See  fig.  24.) 

The  anterior  surface  of  the  chest,  and  the  root  of  the  neck,  have  for 
facihty  of  description  and  for  chnical  convenience,  been  artificially  divided 
into  the  following  regions  : — 

The  supra-sternal,  upper  sternal,  and  lower  sternal  regions,  in  the 
middle  line.  The  supra-clavicular,  clavicular,  infra-clavicular,  mammary 
and  infra-mammary  regions,  on  each  side. 

The  boundaries  of  these  regions  are  as  follows  : — 


96 


Diseases  of  the  Heart. 


The  supra-sternal  region  (i.  fig.  24)  is  situated  immediately  above 
the  upper  end  of  the  sternum,  and  is  bounded  on  each  side  by  the  anterior 
borders  of  the  sterno-mastoid  muscles  ;  its  upper  boundary  corresponds 
to  the  upper  end  of  the  trachea. 

The  upper  sternal  region  (2.  fig.  24)  comprises  the  part  of  the  chest 
which  is  situated  behind  the  upper  portion  of  the  sternum.  The  upper 
boundary-  of  this  region  is  represented  on  the  surface  of  the  chest  by  the 
upper  end  of  the  sternum,  the  lower  end  by  a  line  drawn  across  the 
sternum  at  the  level  of  the  junction  of  the  third  costal  cartilages  ;  laterally 
this  region  is  bounded  on  each  side  by  the  corresponding  edge  of  the 
sternum. 


Fig.   2i,.  —  The  regions  on  the  front  of  the  Chest.     (Modified  after  Walshe.) 

1.  Supra  sternal  region. 

2.  Upper  sternal  region. 

3.  Lower  sternal  region. 

4>4''  Right  and  left  supra-clavicular  regions. 

5' 5'-  Right  and  left  clavicular  regions. 

6,6'.  Right  and  left  infra-clavicular  regions. 

7j7'-  Right  and  left  mammary  regions. 

8,8'.  Right  and  left  infra-mammary  regions. 


Relationship  of  t lie  Heart  to  the  Chest  Wall.       97 

The  lower  sternal  region  (3.  fig.  24)  corresponds  to  the  lower  portion  of 
the  sternum. 

TJie  supra-clavicular  region  (4  and  4'.  fig.  24)  is  triangular  in  shape, 
and  is  situated  immediately  above  the  clavicle  ;  on  its  inner  side  it  is 
bounded  by  the  outer  side  of  the  supra-sternal  region,  below  by  the  clavicle; 
its  third  side  being  formed  by  an  artificial  fine  drawn  from  the  outer  end  of 
the  clavicle  to  the  upper  end  of  the  trachea. 

TJie  clavicular  region  (5  and  5'.  fig.  24)  corresponds  to  the  inner  half 
of  the  clavicle. 

The  infra-clavicular  region  (6  and  6 '.  fig.  24)  is  bounded  above  by 
the  clavicle  ;  below  by  a  fine  drawn  across  the  chest  on  the  level  of  the 
third  rib  ;  internally  by  the  edge  of  the  sternum  ;  externally  by  an  imagi- 
nary line  falling  vertically  from  the  inner  edge  of  the  acromial  process. 

TJie  mani)nary  region  (7  and  7 '.  fig.  24)  is  situated  immediately 
below  the  infra-clavicular  region  ;  and  is  bounded  below  by  a  slanting 
line  drawn  through  the  middle  of  the  sixth  costal  cartilage  ;  internally 
by  the  edge  of  the  sternum  ;  and  externally  by  the  vertical  '  acromial 
line '  described  above. 

The  infra-mammary  region  (8  and  8'.  fig.  24)  is  situated  immediately 
below  the  mammary  region  ;  its  lower  margin  corresponds  to  the  lower 
margins  of  the  false  ribs  ;  internally  it  is  bounded  by  the  edge  of  the 
sternum,  and  below  that  bone  by  the  margins  of  the  ribs  ;  externally  by 
the  'acromial  line.' 

The  exact  relationship  of  the  cardiac  cavities  to  the  front  of  the  chest  is, 
according  to  Walshe,  as  follows  : — The  anterior  surface  of  the  heart  is 
chiefly  formed  by  the  right  cavities ;  the  tip  of  the  left  auricular 
appendix,  and  a  narrow  strip  of  the  left  ventricle  being  the  only  parts  of 
the  left  heart,  which  are  visible  when  the  anterior  surface  is  exposed  in  situ. 

The  right  auricle  reaches  into  the  right  mammary  region,  mainly  on  the 
level  of  the  third  cartilage  and  fourth  interspace,  slightly  on  that  of  the 
second  space. 

The  right  ventricle  corresponds  mainly  to  the  lower  sternal  and  left 
mammary  regions,  its  inferior  and  nearly  horizontal  border  stretching 
from  the  fifth  right  cartilage  to  the  point  at  which  the  apex  beats. 

The  left  auricle  lies  deeply  behind  the  root  of  the  pulmonary  artery, 
little  but  the  appendix  being  visible. 

The  left  vetitricle  extends  vertically  from  the  third  to  the  upper  edge  of 
the  sixth  left  costal  cartilage,  and  occupies  a  portion  of  the  left  mammary 
region — a  comparatively  narrow  strip  being  visible  anteriorly. 

The  entire  of  the  left  ventricle,  the  greater  part  of  the  left  auricle,  and 
a  large  portion  of  the  right  ventricle  towards  the  apex,  lie  to  the  left  of 
the  sternum.  On  the  level  of  the  fourth  cartilage  the  widths  of  the  heart 
substance  lying  on  either  side  of  the  left  border  of  the  sternum  are  very 
closely  the  same.^ 

'  Diseases  of  the  Heart,  p.  4. 

G 


98  Diseases  of  the  Heart. 

Method  of  inspecting-  tJie  Clwst. 

The  patient  should  be  stripped  to  the  waist,  and  placed 
directly  opposite  the  observer,  in  a  good  light,  in  a  sitting 
or  semi-recumbent  position.  In  cases  of  suspected  aneurism, 
in  which  it  is  important  to  note  the  slightest  elevation  of  the 
chest-wall  above  the  level  of  surrounding  parts,  the  suspected 
region  of  the  chest  must  be  well  illuminated,  and  the  observer 
having  placed  himself  on  the  opposite  side  of  the  patient  to 
that  from  which  the  rays  of  light  are  proceeding,  should 
bring  his  eye  to  the  same  horizontal  plane  as  the  region  of 
the  chest  which  he  wishes  to  examine.  In  this  manner  slight 
local  elevations  can  be  most  readily  observed. 

Tlie  points  to  be  observed  in  i)ispccting  the  prceeordial  region 
are  : 

1.  Its  form  and  conformation. 

2.  The  position,  extent,  and  character  of  the  visible  im- 
pulse, especially  the  position  of  the  apex  beat. 

3.  The  condition  of  the  integument.  (This  is  a  point  of 
comparatively  little  importance). 

TJie  form  and  eonformation  of  tJie preeeordial  region. 

In  health  the  two  sides  of  the  chest  are  practically  sym- 
metrical, and  the  left  mammary  region  does  not  differ  in  form 
and  shape  from  the  corresponding  region  on  the  opposite  side. 

Alterations  in  the  form  and  conformation  of  the  praecordial 
region  are  frequently  met  with  in  disease ;  in  some  cases  it 
is  unduly  prominent,  in  others  it  is  flattened  or  retracted. 

Undue  prominenee  of  the  prcveordial  region. 

This  condition  may  be  due  to  : 

I.  Congenital  or  acquired  alterations  in  the  shape  of  the 
thorax,  such  as  are  seen  in  some  cases  of  rickets,  or  in  con- 
nection with  some  curvatures  of  the  spinal  column. 

Diagnosis. — In  these  cases  the  character  of  the  prominence  ;  the 
presence  of  other  associated  alterations  in  the  bony  walls  of  the  thorax, 
such  as  a  well-marked  spinal  curvature  ;  and  the  history  of  the  case,  enable 
us  without  difficulty  to  determine  the  cause  of  the  prominence. 


Undue  proviinencc  of  the  Prcccordial  Region.      99 

2.  Abnormal  conditions  of  the  thoracic  parieties  in  the 
praicordial  region,  such  as  an  abscess  in  the  subcutaneous 
cellular  tissue,  or  an  exostosis,  or  other  new  formation  spring- 
ing from  the  ribs  or  cartilages. 

Diagnosis. — In  these  cases — which  are  rare — the  diagnosis  presents  no 
difficulty. 

In  the  case  of  an  abscess  in  the  chest  wall  there  is  tenderness  on 
pressure  over  the  swelhng,  and  often  redness  of  the  skin  of  the  affected 
part  ;  the  history  shows  a  recent  origin,  and  there  are  no  signs  of  disease 
of  the  subjacent  viscera. 

Solid  tumours  springing  front  the  ribs  or  cartilages  are  also  unattended 
by  evidence  of  cardiac  or  puhiionary  disease  ;  they  are  usually  well 
defined  and  localised,  and  are  as  a  rule  readily  distinguished,  by  means 
of  palpation,  from  all  other  causes  of  bulging. 

3.  Fluid  accumulations  in  the  left  pleural  sac  ;  solid 
tumours  of  the  left  lung ;  solid  tumours  in  the  anterior 
mediastinum. 

Diagnosis. — Fluid  accumulations  in  the  left  pleural  sac,  which  give 
rise  to  prominence  of  the  pracordia,  also  produce  bulging  of  the  whole  ^  of 
the  affected  (left)  side,  and  are  attended  by  the  characteristic  symptoms 
and  signs  of  left  pleural  effusion. 

Solid  tumours  of  the  left  lung,  and  new  growths  in  the  mediastinum, 
seldom  give  rise  to  marked  prominence  of  the  prsecordia.  When  sufficiently 
large  to  produce  bulging  of  this  part  of  the  chest  wall,  they  are  attended 
with  characteristic  symptoms  and  signs,  which  it  would  be  out  of  place 
to  enumerate  here. 

4.  Fluid  in  the  sac  of  the  pericardium. 

5.  Increase  in  the  size  of  the  heart  itself,  especially  those 
enlargements  which  are  attended  with  marked  hypertrophy 
of  the  organ. 

The  characteristic  features  of  prominence  of  the  prae- 
cordia,  due  to  fluid  in  the  sac  of  the  pericardium  and 
enlargement  of  the  heart  itself,  which  are  the  most  common 
causes  of  local   bulging,  and  which   are  of  course  the  most 

'  A  small  encysted  pleuritic  effusion  might  produce  local  bulging  of  the  prse- 
cordia  ;  but  such  a  condition  is  infinitely  rare.  A  more  frequent  condition,  but 
one  which  seldom  gives  rise  to  difficulties  in  diagnosis,  is  an  empyema  which  is 
pointing. 


loo  Diseases  of  tJie  Heart. 

important,  so  far  as  our  present  studies  are  concerned,  will 
be  afterwards  considered  in  detail.  It  is  important  to 
remember  that  the  prominence  which  results  from  these 
causes  is  greater  in  young  persons  (in  whom  the  chest  walls 
are  elastic)  than  in  old  people. 

6.  Forward  displacement  of  the  heart  by  an  aneurismal 
or  solid  tumour  situated  behind  it.  This  condition  is  ex- 
tremely rare. 

7.  The  presence  of  an  aneurism  of  the  first  portion  of  the 
aortic  arch.  The  bulging  in  such  cases  is  almost  invariably 
above  the  fourth  rib,  but  occasionally  the  aneurism  '  points ' 
lower  down,  as  in  a  case  which  I  shall  afterwards  describe. 

Flattening  or  retraction  of  tJie precordial  region. 

This  condition  may  be  due  to  : 

1.  Congenital  malformation. 

Diagnosis. — In  these  cases  the  depression  is  seldom  limited  to  the 
prsecordial  region.  It  is  usually  symmetrical,  and  involves  the  lower 
sternal  region,  together  with  more  or  less  of  the  mammary  and  infra-mam- 
mary regions  on  each  side. 

2.  Long  continued  external  pressure.  Depression  of  the 
lower  end  of  the  sternum  is  sometimes  seen  in  shoemakers, 
and  is  produced  by  the  pressure  of  the  '  last '  against  this 
part  of  the  chest. 

Diagnosis. — The  depression  which  occurs  in  shoemakers  is  more  cen- 
tral than  the  depression  which  results  from  cardiac  affections,  and  in- 
volves the  right  as  well  as  the  left  infra-mammary  region.  The  central 
position  of  the  depression  and  the  nature  of  the  patient's  employment, 
together  with  the  absence  of  any  history,  symptoms,  or  signs  of  local 
disease,  are  the  points  to  which  attention  must  be  directed  in  making  the 
diagnosis. 

3.  Retraction  of  the  left  lung,  a  condition  which  may 
result  from  pleurisy,  cirrhosis  of  the  lung,  etc. 

Diagnosis. —  In  these  cases  the  retraction  or  depression  is  not  con- 
fined to  the  praecordial  region,  but  affects  the  whole  of  the  left  side  ;  while 
the  associated  physical  signs,  and  the  previous  histor}',  usually  afford 
distinctive  evidence  of  the  condition. 


The  Visible  Impulse  of  the  Heart.  loi 

4.  Pericarditis. — Here  the  depression  is  usually  confined 
to  the  lower  end  of  the  sternum  and  the  adjacent  part  of  the 
left  infra-mammary  region.  The  depression  does  not  occur 
until  absorption  of  the  inflammatory  products,  and  adhesion 
of  the  opposed  surfaces  of  the  pericardium  have  taken  place. 
It  is  always  best  marked  in  those  cases  in  which  the  chest 
wall  is  elastic  {i.e.  in  young  subjects),  and  in  which  the  ex- 
terior of  the  pericardium  has  become  adherent  to  the  chest 
wall  as  the  result  of  inflammation  outside  the  sac. 

The  position,  extent,  and  charaetcr  of  the  Visible  Impulse, 
espeeially  the  position  of  the  Apex  Beat. 

The  visible  impulse  as  a  whole,  and  the  position  and 
characters  of  the  apex  beat  in  particular,  must  be  noted — 
but  since  it  is  usually  necessary  to  confirm  and  supplement 
the  information  derived  from  inspection  by  means  of  pal- 
pation, I  shall  leave  the  description  of  the  cardiac  impulse  in 
health  and  in  disease  until  that  method  of  investigation  has 
been  considered. 

Epigastric  Pulsation. 

Should  this  condition  be  present,  it  will  of  course  be 
observed  at  this  stage  of  the  examination  {i.e.  during  the 
inspection  of  the  praecordial  region)  ;  but  since  it  is  necessary 
to  employ  palpation  to  define  its  exact  characters,  it  will  be 
more  conveniently  considered  after  that  mode  of  examination 
has  been  described. 

Pulsations  over  the  Aorta  and  at  the  Root  of  the  Neck. 

In  addition  to  the  visible  cardiac  impulse  and  the 
epigastric  pulsation  just  mentioned,  the  presence  or  absence 
of  pulsation  in  other  parts  of  the  thorax  and  at  the  root  of 
the  neck  should  be  noted  at  this  stage  of  the  examination. 
It  will,  however,  be  more  convenient  to  describe  these  pul- 
sations when  I  come  to  treat  of  the  systematic  examination 
of  the  aorta  and  superficial  vessels. 


I02  Diseases  of  the   Heart. 

The  Condition  of  the  Integument  over  the  Pmeordia. 

The  condition  of  the  integument  over  the  prsecordial 
region  sometimes  affords  useful  information. 

Cupping  marks  are  suggestive  of  previous  inflamma- 
tion ;  and  a  history  of  cupping  during  a  previous  attack 
of  rheumatic  fever  is  very  suggestive  of  an  acute  rheu- 
matic inflammation  of  the  heart  (pericarditis,  or  endo- 
carditis). 

Prcecordial  Vascularity.  —  It  is  common  to  observe, 
especially  after  middle  life,  a  line  of  minute  vessels  running 
across  the  chest  in  the  neighbourhood  of  the  praecordial  region. 
The  late  Professor  Laycock,  who  first  directed  attention  to 
the  condition,  considered  that  it  Avas  suggestive  of  cardiac 
disease,  and  there  can  be  no  question  but  that  the  condition 
is  more  frequent  in  persons  suffering  from  vascular  lesions 
than  in  other  people,  but  it  occurs  not  unfrequently  in 
perfectly  healthy  individuals,  and  is  not  therefore  a  sign  of 
much  importance. 

CEdcjna  of  the  subcutaneous  cellular  tissue,  when  it  is 
limited  to  the  praecordial  region,  usually  depends  upon  a  local 
inflammation,  and  is  then  associated  with  tenderness  on 
pressure,. redness,  and  the  like.  It  may  however  depend  upon 
disease  of  the  subjacent  viscera.  The  condition  with  which 
it  is  most  frequently  associated  is  a  malignant  intra-thoracic 
growth.  Oedema  of  the  chest  wall  and  of  the  praecordial  region 
is  also  of  course  seen  as  part  and  parcel  of  a  general  dropsy. 

PALPATION    OF   THE    PR/ECORDIA. 

Palpation  corroborates  the  information  derived  from  in- 
spection, and,  in  many  cases,  enables  us  to  ascertain  with 
exactitude : — 

1.  The  position  of  the  apex  beat. 

2.  The  character  of  the  cardiac  contractions,  i.e.  the  force, 
rhythm,  celerity,  etc.,  of  the  cardiac  impulse. 

In  some  cases  it  also  affords  additional  information,  in- 
asmuch as  it  reveals  the  presence  of  cardiac  thrills,  or  friction 
fremitus,  and  enables  us  to  elicit  the  presence  or  absence  of 
pain  and  tenderness  on  pressure  over  the  praecordial  region. 


Palpation.  103 

Method  of  palpating  the  Chest  in  order  to  ascertain  the  exact 
position  of  the  Apex  Beat. 

In  order  to  ascertain  the  exact  position  of  the  apex  beat 
by  means  of  palpation,  the  patient  should  be  laid  in  the  re- 
cumbent position,  and  the  fingers  of  the  right  hand  placed 
lightly  over  the  front  of  the  chest  below  the  left  nipple. 
The  position  of  maximum  cardiac  impulse,  which  usually 
corresponds  to  the  position  of  the  apex  beat,  should  then  be 
noted,  and  the  interspace  in  which  the  apex  pulsation  is 
situated,^  and  the  distance  of  the  apex  beat  from  the  left 
border  of  the  sternum  ascertained. 

It  sometimes  happens  that  the  apex  beat  is  not  ap- 
preciable when  the  patient  is  in  the  recumbent  position.  In 
these  cases  (the  nature  of  which  I  will  presently  describe),  the 
position  of  the  apex  beat  can  usually  be  ascertained  by  so 
altering  the  position  of  the  patient  as  to  bring  the  heart 
more  in  contact  with  the  wall  of  the  chest.  He  may  be  made 
to  sit  up  and  to  lean  forward,  for  instance  ;  or,  he  may  be 
placed  on  his  left  side.  If  the  latter  method  be  adopted,  due 
allowance  must  be  made  for  the  lateral  displacement  of  the 
heart,  which  results  from  the  alteration  in  position."^ 


'  To  ascertain  the  exact  position  of  the  apex,  the  interspaces  must  be  carefully 
counted  from  above  downwards  ;  the  forefinger  of  the  right  hand  should  first  be 
made  to  define  the  position  of  the  first  interspace  immediately  below  the  clavicle 
(in  many  persons  there  is  a  well  marked  prominence  of  the  sternum  at  the  level  of 
the  second  costal  cartilages,  which  forms  an  easy  guide  to  the  second  interspace) ; 
the  middle  finger  of  the  same  hand  should  then  be  inserted  between  the  second 
and  third  ribs  ;  the  second  interspace  having  thus  been  ascertained,  the  forefinger 
of  the  right  hand  should  be  placed  in  it,  and  the  middle  finger  should  then,  but 
not  till  then,  be  slipped  over  the  third  rib  into  the  third  interspace  ;  the  fourth 
and  succeeding  interspaces  are  successively  defined  in  the  same  manner,  until  that 
in  which  the  apex  beat  is  situated,  is  finally  reached.  The  position  of  the  apex 
with  regard  to  the  left  nipple  (in  males)  ;  or,  better,  its  exact  distance  from  the 
left  border  of  the  sternum,  must  then  be  measured  and  noted. 

Note. — In  fat  or  very  muscular  persons  it  may  be  necessary  to  use  some  force 
in  defining  the  position  of  the  interspaces  in  the  manner  just  described. 

^  According  to  Sibson,  the  apex  beat  may,  in  some  cases,  be  displaced  as 
much  as  two  inches  to  the  left,  by  turning  the  patient  from  the  back  on  to  his  left 
side. 


I04  Diseases  of  the  Heart. 

The  position  of  the  apex  beat  is  of  great  practical  import- 
ance, for  it  corresponds  to  the  lowest  point  of  the  heart,  and 
is  in  fact  the  means  by  which  we  are  in  the  habit  of  deter- 
mining the  lower  boundar}-  of  the  organ. 

TJie  jionnal position  of  the  apex  beat. 

In  the  adult  healthy  male  the  apex  can  usually  be  seen 
and  felt  pulsating  (over  an  area  about  an  inch  square)  be- 
tween the  fifth  and  sixth  ribs,  at  a  point  two  inches  to  the 
left  of  the  sternum.^  In  well  nourished  healthy  persons,  the 
apex  pulsation  is  the  only  pulsation  which  is  visible  over  the 
praecordia  during  ordinary  (tranquil)  action  of  the  heart. 

In  women  with  well  developed  mammae,  in  fat  or 
muscular  persons,  and  when  the  heart  is  acting  feebly  the 
apex  beat  may  be  invisible.  Viee  ve7'sd,  in  thin  persons,  or 
where  the  heart  is  excited  or  h)'pertrophied,  the  apejc  beat  is 
unusually  well  marked. 

The  position  of  the  apex  beat  varies  somewhat  in 
different  healthy  individuals,  being  sometimes  situated  a 
little  higher,  sometimes  a  little  lower  than  the  fifth  inter- 
space. These  alterations  depend  for  the  most  part,  as  Sibson 
has  shown,  upon  the  length  of  the  arch  of  the  aorta ;  and  also 
upon  the  age  of  the  individual,  the  form  of  the  thorax,  and 
the  condition  of  the  respiratory  organs. 

In  children  the  apex  beat  is  usually  higher,  and  often 
more  to  the  left ;  rice  versd,  in  old  people,  and  especially  in 
those  in  whom  the  aorta  is  atheromatous  and  elongated, 
the  heart,  and  therefore  the  apex  beat,  are  lower  than  the 
fifth  interspace. 

In  strong  robust  persons,  and  in  those  who  possess  a  broad 
and  deep  chest  of  the  inspiratory  type,  the  position  of  the 
heart  and  arteries,  and  of  all  their  parts,  is  lower,  while  in 
those  who  are  slender,  and  possess  a  narrow  and  flat  chest  of 

In  describing  the  position  of  the  apex  beat,  more  particularly  in 
females,  the  interspace  in  which  it  is  situated,  and  its  exact  distance  from 
the  left  border  of  the  sternum  should  be  stated.  In  males  the  apex  beat  is 
normally  situated  an  inch  within,  and  an  inch  or  an  inch  and  a  half  below  the  left 
nipple. 


Congenital  displacements  of  the  Heart.  105 

the  expiratory  type,  the  position  of  these  parts  is  higher  than 
in  the  average  healthy  individual.^ 

During  inspiration  the  apex  beat  (in  its  relationship  to  the 
chest  wall)  is  lower  than  during  expiration.  This  is  partly 
due  to  the  fact,  that  the  heart  descends  with  the  descent  of 
the  diaphragm,  and  partly  because  the  front  wall  of  the  chest 
is  raised  during  inspiration. 

Congenital  displaccinchts  of  the  Heart. 

The  heart  is  occasionally  placed  in  the  right  side  of  the 
chest,  the  apex  beat  being  somewhere  in  the  neighbourhood 
of  the  right  nipple.  When  this  condition  occurs  congenitally, 
there  is  usually  complete  transposition  of  the  viscera,  the 
heart  being  placed  on  the  right  side,  and  the  liver,  for  ex- 
ample, on  the  left  side  of  the  body.  Cases  of  this  description 
are  not  very  uncommon,  and  two  examples  have  come  under 
my  own  personal  observation. 

A  much  rarer  form  of  congenital  displacement  is  that  in 
which  the  heart  is  placed  on  the  right  side,  while  the  liver 
and  other  viscera  are  situated  in  their  usual  position.  The 
following  case  of  this  description  recently  came  under  my 
notice  ;  and  another  case — verified  by  post-mortem  ex- 
amination— has  lately  been  recorded  in  the  pages  of  the 
Lancet? 

Case  I.—  Congenital  displacement  of  the  heart  to  the  right  side,  tJte  position 
of  the  otJier  viscera  being  normal. 

J.  A.,  set.  39,  a  joiner,  presented  himself  at  the  Cowgate  Dispensary, 
Edinburgh,  in  December  1881,  suffering  from  a  dislocation  of  the 
shoulder.  On  stripping  him,  the  house  surgeon  (Dr  Christie)  noticed 
strong  pulsation  just  above  the  right  nipple— while  the  impulse  of  the 
heart  could  not  be  felt  in  the  usual  position.  Concluding  that  the  case 
was  one  of  congenital  displacement  Dr  Christie  kindly  asked  me  to  see 
the  case  ;  and  with  his  opinion  I  entirely  concurred. 

The  facts  which  I  elicited  were  as  follows : — The  patient,  who  was  some- 
what thin  and  of  bad  physique.,  stated,  that  he  had  always  enjoyed  good 

'  Sibson  On  the  Position  ami  Form  of  the  Heart.  Russell  Reynold's  System  of 
Medicine,  vol.  iv.  p.  97. 

■  Lancet,  July  8th,  1882,  p.  9. 


io6 


Diseases  of  tJic  Heart. 


health;  that  he  had  never,  to  his  knowledge,  had  anything  the  matter  with 
his  chest.  He  was  not  short  of  breath,  had  never  sufifered  from  palpita- 
tion or  pain  in  the  region  of  the  heart,  and  had  never  had  any  symptoms 
or  sensations  which  made  him  suspect  that  there  was  anything  wrong 
with  his  heart. 

The  left  infra-mammary  region  looked  flattened,  the  depression  being 
greatest  in  the  sixth  and  seventh  interspaces.  The  heart  impulse  could 
not  be  felt  in  the  usual  position.  On  percussion  the  left  infra-mammarj' 
region  was  hyper-resonant;  and  the  normal  cardiac  dulness  could  not  be 
detected.  The  respiratory  murmur  was  audible  over  the  usual  position  of 
the  heart,  but  the  heart  sounds  could  not  be  heard. 

Very  distinct  pulsation  could  be  seen  and  felt  in  the  third,  fourth, 
and  fifth  right  interspaces  (see  fig.  25)  ;  there  was  marked  dulness  over 
the  area  of  pulsation;  and  the  heart  sounds  were  loudly  heard  over  the 
same  part  of  the  chest.  The  percussion  note  over  the  outer  part  of  the 
right  infra-clavicular  region  was  impaired,  but  the  right  lung,  both  ante- 
riorly and  posteriorly,  seemed  normal.  The  li\er  was  situated  on  the 
right  side;  and  the  stomach  in  its  normal  position — no  splenic  dulness 
was  detectable.  The  girth  of  the  right  side  of  the  chest  was  considerably 
larger  than  that  of  the  left,  the  measurements  being  as  follows : — 


Position  of  Measurement 

At  the  level  of  the  second  rib 

Through  the  nipples        .         .         .         . 

At  the  level  of  the  seventh  rib 

The  heart's  action  was  readily  excited, 
tuated,  but  free  from  murmur. 


Right. 

Left 

16X  in. 

I5>^  in. 

i^Yz  in. 

ilYz  in. 

15      in. 

14      in. 

Both  sounds  were  accen- 


FlG.   25.—  Front  view  oj  the  thorax  in  the  case  of  J.  A. ,  sho'coing  the  area  of 
cardiac  pulsation. 


Displaccuicnts  of  the  Heart.  107 

Diagnosis. — The  heart  was  obviously  placed  on  the  right  side  of  the 
chest.  The  facts,  that  there  was  no  history  or  evidence  of  lung  disease, 
and  that  the  girth  of  the  right  chest  was  considerably  greater  than  the 
left  seemed  to  show  that  the  displacement  was  not  due  to  retraction  of 
the  right  lung,  but  that  it  was  in  all  probability  a  congenital  condition. 
The  peculiarity  of  the  case  consisted  in  the  fact,  that  the  heart  was  the 
only  organ  transposed,  the  liver  and  stomach  being  placed  in  their 
normal  positions.' 

Alterations  in  t/ic position  of  the  Heart  and  Apex  Beat  winch 
oecnr  in  disease. 

In  studying  the  alterations  in  the  position  of  the  apex  beat 
which  occur  in  disease,  it  is  important  to  remember  that  the 
organ  rests  upon  the  diaphragm,  to  which  it  is  indirectly 
attached  by  means  of  the  pericardium,  and  that  it  is  directly 
attached  at  its  base  to  the  great  vessels,  and  behind  to  the 
roots  of  the  lungs  by  the  pulmonary  veins. 

The  organ  therefore  ascends  and  descends  with  the  ascent 
and  descent  of  the  diaphragm  ;  further,  it  is  readily  displaced 
from  side  to  side  by  lateral  pressure. 

The  alterations  in  the  position  of  the  heart  and  apex  beat 
which  result  from  disease,  may  be  due  either  to  extrinsic  or 
intrinsic  canses. 

A.    Displacement  of  the  Heart  dice  to  extrinsic  canses. 

The  heart  may  be  pnsJied  to  one  side  by  fluid,  gaseous,  or 
solid  accumulations  or  by  enlargements  of  the  surrounding 
viscera  ;  or,  it  may  he  pnlled^  to  one  side  by  retraction  of  the 
air  containing  viscera,  i.e.  the  lungs  ;  or,  again,  it  may,  by  the 
force  of  gravity,  fall  with  the  descent  of  the  diaphragm.^ 

'  Breschet  and  Otto,  quoted  by  Peacock,  in  his  work  on  Alalformaiions  of  the 
Hitman  Heart,  page  2,  have  met  with  cases  of  this  description  ;  but  so  far  as  I 
have  been  able  to  ascertain,  no  other  cases  have  been  recorded  in  English 
medical  literature. 

-  The  contraction  of  the  lung  tends  to  produce  a  vacuum  within  the  thorax,  in 
consequence  of  which  the  adjacent  organs,  including  the  heart,  are  of  course 
displaced  (pushed  rather  than  pulled)  towards  the  affected  side  by  the  atmospheric 
pressure. 

'  When  the  diaphragm  descends,  the  great  vessels  (and  therefore  the  heart) 
are  also  dragged  down  by  reason  of  their  attachment  to  the  pericardium. 


io8 


Diseases  of  the  Heart. 


The  displacement  may  be  either  to  the  right  or  to  the  left, 
upwards  or  downwards,  forwards  or  backwards. 

Displacement  of  the  Heart  and  Apex  Beat  to  the  right  may 
be  due  to  : — 

1.  The  presence  of  fluid,  gaseous,  and  solid  accumulations 
in  the  left  pleural  sac,  or  solid  enlargements  of  the  left  lung. 

2.  Retraction  of  the  right  lung — a  condition  which  usually 
results  from  pleurisy  with  effusion,  cirrhosis  or  phthisis. 

Fluid  in  the  left  pleural  sac   (see  fig.  26)  is  by  far   the 
most  common  cause  of  displacement  to  the  right ;  and   in 


Fig.   26. — Displacement  of  the  heart  to  the  right  as  the  result  0/  effusion  into  the 
left  pleural  cavity.     {Modified  froin  Sib  son.) 

these  cases  the  apex  beat  not  unfrequently  corresponds  to 
the  right  nipple.  Extreme  displacement  to  the  right  may 
also  be  due  to  retraction  of  the  right  lung.  Sibson  quotes 
several  cases  of  this  description,^  and  I  have  seen  more  than 
one  case  in  which  the  pulsation  of  the  heart  was  situated  just 
above  the  right  nipple. 


'  Russell  Reynold's  System  of  Medi.inc,  vol.  iv.  p.  143. 


Displacements  of  the  Heart. 


109 


Displacciiieni  of  the  heart  and  apex  beat  to  the  left  may 
be  due  to  : 

1.  Accumulation  of  fluid,  gaseous,  or  solid  matter  in  the 
right  pleural  cavity  ;  or  solid  enlargements  of  the  right  lung 
or  right  lobe  of  the  liver. 

2.  Retraction  of  the  left  lung  (see  fig.  27). 


Fig.   27. — Displaceminit  of  the  heart  to  the  left,  in  consequence  of  retraction 
{cirrhosis)  of  the  left  lung.      (Modified  from.  Sibson.) 

The  displacement,  which  results  from  this  cause  is  seldom 
so  great  as  in  the  following  case,  in  which  the  pulsations  of 
the  heart  were  observed  in  the  left  axilla. 

Case  If. — Pleurisy  :  Cirrliosis  {?)  of  the  left  Lung;  great  displacement  of 
tlie  Jieart  to  the  left. 

J.  M.,  set.  21,  a  fireman,  was  admitted  to  the  Ne\vcastIe-on-Tyne 
Infirmary,  under  my  care,  on  3d  December  1874,  complaining  of  palpita- 
tion, shortness  of  breath,  cough,  spit,  and  great  debility. 

Previous  history. — The  patient,  who  has  always  been  very  round 
shouldered,  stated  that  he  had  enjoyed  excellent  health  until  four  years 
ago,  when  he  had  an  attack  of  rheumatic  fever,  which  laid  him  up  for 
fourteen  weeks  :  he  does  not  know  whether  his  heart  was  affected  or  not. 
After  this  attack  he  enjoyed  good  health  for  some  years,  when  he  '  caught 
a  severe  cold,'  in  consequence  of  exposure  to  cold  and  wet,  and  was  ill  for 
several  weeks  with  cough  and  severe  pain  in  the  left  side,  which  '  caught 


no  Diseases  of  tJic  Heart. 

his  breath.'  These  symptoms  gradually  subsided,  and  he  continued  in 
excellent  health  until  four  months  ago,  when  his  present  illness  com- 
menced with  cough,  spit,  and  shortness  of  breath.  These  symptoms  have 
gradually  increased,  and  he  has  lost  a  great  deal  of  flesh. 

Presetit  condHion—ViQ  is  considerably  emaciated.  The  girth  of  the 
left  chest  is  considerably  less  than  that  of  the  right,  the  measurements 
being  as  follows  : — 

Position  of  measurement.  Right.  Left 

At  the  second  rib i5>^  in.         \i\)i'm. 

At  the  nipples I5/^  i"-  I4/^  in- 

At  the  ensiform  cartilage        .         .         .  15       in.  1 5       in. 

The  percussion  note  over  the  greater  part  of  the  left  lung,  but  especi- 
ally at  the  base,  is  impaired  ;  increased  vocal  resonance,  sibilant  rales, 
and  occasional  large  crepitations  are  heard  on  auscultation.  There  was 
also  evidence  of  commencing  consolidation  of  the  right  apex.  The  pul- 
sation of  the  heart  can  be  very  distinctly  seen  and  felt  in  the  left  axillary 
and  infra-axillary  regions,  the  apex  being  apparently  situated  in  the 
sixth  interspace,  two  inches  outside  the  nipple.  The  percussion  note 
between  the  left  nipple  and  the  sternum  is  resonant,  and  the  heart  sounds 
are  inaudible  at  this  spot  ;  at  the  aortic  cartilage  the  heart  sounds  are 
ver^f  faint,  but  are  much  louder  in  the  second  and  third  interspaces  on  the 
left  side. 

Upward  displacement  may  be  due  to  : 

(i)  Anything  which  raises  the  arch  of  the  diaphragm,  such 
as  soHd,  Hquid,  or  gaseous  accumulations  in  the  cavity  of  the 
abdomen — ascites  (see  fig.  28),  ovarian  tumours,  tympanites, 
enlargement  of  the  Hver  (see  fig.  29),  fibroid  tumours  of  the 
uterus,  etc. 

In  many  of  these  cases  the  displacement  is  partly  to  one 
side  as  well  as  upwards.  Enlargement  of  the  left  lobe  of 
the  liver,  for  example,  usually  displaces  the  heart  upwards 
and  to  the  left,  while  great  enlargement  of  the  spleen  may 
push  it  upwards  and  to  the  right. 

(2)  Retraction  of  the  upper  part  of  either  lung,  the  most 
common  pathological  condition  being  phthisis. 

Dozvmvard  displacement  may  be  caused   by  : 

(i)  Anything  which  presses  down  the  heart  or  diaphragm, 

such  as  aneurisms  or  solid  tumours,  emphysema  of  the  lungs, 

etc.  (see  fig.  30). 


Displacements  of  the  Heart. 


1  1 1 


Fig.   28.  —  Upivard  displacement  of  the  heart,  the  result  of  ascites. 

(2)  Collapse  of  the  abdominal  viscera,  and  consequent 
descent  of  the  diaphragm. 

Forivard  displacement  is  very  rare,  but  it  does  sometimes 
result  from  an  aneurism  (as  in  a  case  which  I  shall  afterwards 
relate)  or  a  solid  tumour  in  the  posterior  mediastinum. 

Backivard  displacement  is  still  more  rare  ;  it  is  said  to  be 
occasionally  produced  by  tumours  or  inflammatory  accumu- 
lations in  the  anterior  mediastinum,  but  no  case  of  this 
description  has  come  under  my  personal  observation. 


I  12 


Diseases  of  the  Heart. 


Fig.   29. — Displacement  of  the  heart  ufncards  and  to  the  left,  the  result  of 
enlargement  of  the  liver.     {Modified  frotn  Sibson. ) 


Fig.  30. — Do7vnward  displacement  of  the  heart,  the  result  ofpithnonary  emphysema. 
( After  Sibson,  modified. ) 


Displacements  of  tJie  Heart.  1 13 

B.  Displacements  of  the  apex  beat  due  to  intrinsic  causes. 
The  intrinsic  conditions  which  may  produce  displacement 
of  the  heart  and  apex  beat  are  — 

1.  Fluid  in  the  sac  of  the  Pericardium. — Where  the  peri- 
cardial effusion  is  considerable,  but  not  excessive,  the  base  of 
the  heart  and  the  great  vessels  are  pushed  upwards  and 
backwards,  and  the  apex  is  tilted  upwards  and  outwards,  so 
that  it  may  correspond  in  position  to  the  left  nipple,  or  in 
some  cases  may  be  situated  still  further  to  the  left. 

Where  the  effusion  is  very  copious,  the  apex  beat  may  be  completely 
obscured  ;  while  in  those  cases  in  which  the  amount  of  effusion  is  small 
(the  heart  itself  being  of  normal  size),  or  in  which  the  heart  is  fixed  by 
old  pericardial  adhesions,  there  is  little  or  no  alteration  of  the  apex  beat. 

2.  Alterations  in  the  shape  and  size  of  the  heart  itself.- — 
When  the  left  ventricle  is  hypertrophied  (see  fig.  31),  the 
extension  is  chiefly  downwards  and  outwards  {i.e.  to  the  left), 
and  the  apex  beat  may  be  situated  in  the  sixth,  seventh,  or 
even  the  eighth  interspace,  three,  four,  or  even  five  inches  to 
the  left  of  the  sternum.  In  many  cases  it  is  considerably 
outside  the  left  nipple. 

In  hypertrophy  and  dilatation  of  the  right  ventricle,  the 
apex  beat  (which  is  usually  under  such  circumstances  more 
diffused  than  in  health),  is  displaced  downwards  and  to  the 
right  (see  fig.  32),  and  the  cardiac  impulse  is  not  unfrequently 
best  seen  and  felt  in  the  pit  of  the  epigastrium.  But  since 
epigastric  pulsation  may  be  due  to  several  other  important 
conditions,  it  will  perhaps  be  well  to  enumerate  them  here. 

Epigastric  Pulsation. 

The  chief  forms  of  epigastric  pulsation  are,  in  the  order  of 
their  relative  frequency,  as  follows  : 

(i.)  Transmitted  pulsation  from  the  heart. — This  form  of 
pulsation  is  generally  due  to  enlargement  (hypertrophy  and 
dilatation)  of  the  right  ventricle,  but  it  may  also  be  caused 
by  the  downward  displacement  of  the  organ,  which  is  seen  in 
pulmonary  emphysema,^  aneurism  of  the  arch  of  the   aorta, 

'  In  emphysema  the  right  side  of  the  heart  is  dilated  and  hypertrophied,  and 
to  this  cause  the  epigastric  pulsation,  which  is  so  marked  a  feature  in  emphysema, 
is  in  part  due. 

H 


114 


Diseases  of  the  Heart. 


collapse  of  the  abdominal  viscera,  etc.  The  pulsation  is  in 
these  cases  exactl}'  synchronous  with  the  ventricular  contrac- 
tion, and  is  often  transmitted  through  the  left  lobe  of  the  liver. 
(2.)  Pulsation  of  the  abdoniinat  aorta. — In  some  of  these 
cases,  as  for  instance  in  neurotic  pulsation  of  the  vessel,  the 
aortic  pulsation  may  be  directly  felt,  in  others  it  is  indirectly 
felt,  and  is  communicated  through  the  liver  or  some  solid 
body,  such  as  a  cancer  of  the  pylorus,  lying  in  front  of  the 


Fig.  31. — Hypertrophy  of  the  left  veiitiicle,  shoiving  the  altered  positio)i  of  the  apex. 
(After  von  Dusch.) 

The  continuous  line  represents  the  normal  heart ;  the  dotted  line  the  hyper- 
trophied  left  ventricle.  The  apex  of  the  left  ventricle  is  outside  the  dotted  line 
a  b,  which  is  drawn  through  the  left  nipple. 


Displacement  of  the  apex-beat. 


I  I 


vessel.  The  pulsation  in  this  form  is  a  little  behind  (after) 
the  apex  beat,  but  this  fact  is  sometimes  with  difficulty 
established  in  practice. 

(3.)  Aneurisin  of  the  lozt'er  part  of  the  thoracic,  or  of  the 
upper  part  of  the  abdominal  aorta. — This  is  not  a  common 
cause  of  epigastric  pulsation.  The  aneurismal  pulsation  may 
be  directly  felt,  or  may  be  transmitted  through  the  liver. 

According  to  Sibson,  the  epigastric  pulsation,  which  is 
caused  by  an  aneurism  of  the  lower  part  of  the  thoracic  or 


Fig.   32. — Hypertrophy  of  the  right  venti-icle.     (After  von  Dusch.) 

The  normal   outline   of  the  heart  is   represented   by  a  continuous  line  :    the 
hypertrophied  right  heart  by  a  dotted  line. 


1 1 6  Diseases  of  the  Heart. 

the  upper  part  of  the  abdominal  aorta,  is  strong  during  ex- 
piration, but  is  lessened,  or  even  disappears,  during  inspiration. 
In  cases  of  abdominal  collapse,  on  the  contrary,  the  epigastric 
pulsation  is  more  marked  when  the  patient  takes  a  deep  in- 
spiration.^ 

(4.)  True  Pulsation  in  the  liver. — Here  the  pulsation  is 
caused  by  a  '  back-wash  '  from  the  right  auricle.  The  liver 
is  always  enlarged,  and  the  pulsation  is  diffused  through,  and 
not  simply  communicated  to  it.  Its  rhythm  corresponds 
to  tlie  apex  beat,  for  the  blood-wave  which  produces  it  is 
propelled  by  the  right  ventricle  through  the  incompetent  tri- 
cuspid orifice  into  the  hepatic  veins.  This  form  of  pulsation 
is  therefore  pathognomonic  of  tricuspid  regurgitation.  In 
some  cases  of  this  description  the  hepatic  pulsation  may 
possibly  be  due  to  communicated  pulsation  from  the  inferior 
vena  cava,-  for  the  back-wash  also  extends  into  that  vessel. 

THE   EXTENT   OF   THE   CARDIAC   IMPULSE   AS   ASCERTAINED 
BY   INSPECTION   AND    PALPATION. 

In  health,  and  during  tranquil  action  of  the  heart,  the 
apex  beat  is  the  only  cardiac  pulsation  which  is  visible,  and 
it  usually  covers  an  area  of  about  one  square  inch  in  extent. 
When  the  heart  is  excited,  in  thin  persons,  and  when  an 
unusually  large  portion  of  the  organ  is  in  direct  contact  with 
the  chest  wall — a  condition  which  may  result  from  increased 
size  of  the  organ,  forward  displacement  of  the  heart,  or 
retraction  of  the  anterior  margins  of  the  lung — pulsation  may 
be  seen  and  felt  over  a  large  portion  of  the  precordial  region. 
Diffuse  wave-like  pulsation  is  seen  in  some  cases  of  dilatation 
of  the  organ,  and,  according  to  some  observers  ^  in  pericardial 
effusion. 


'   Russell  Reynold's  System  of  Med  id /le,  vol.  iv.  p.  129. 
Pulsation  in  the  vena  cava  might  also  result  from  a  communication  between 
a  large  arterial  trunk,  such  as  the  abdominal  aorta,  and  that  vessel ;  but  I  am  not 
acquainted  with  any  case  in  which  this  condition  has  been  observed. 

'  It  is  very  doubtful  whether  a  diffuse  wave-like  pulsation  over  the  precordial 
region  does  result  from  pericardial  effusion. 


Diniiuished  cardiac  impulse.  1 1  7 

The  exact  character  of  tJie  Cardiac  Impulse  ivith  respect  to 
force,  rhythm,  celerity,  etc. 

The  force  of  the  cardiac  impulse  is  ascertained  by  pal- 
pating the  praecordia  in  the  manner  described  above,  and  is 
still  more  accurately  observed  by  placing  the  right  hand  over 
the  precordial  region,  the  left  hand  over  the  back  between 
the  scapulae,  and  by  compressing  the  chest  firmly  between 
the  two.  The  pulsation  of  deep-seated  aneurisms  can  some- 
times be  observed  by  this  method,  when  the  ordinary  method 
of  palpation  fails  to  elicit  any  abnormal  pulsation. 

The  force  of  the  cardiac  impulse  varies  considerably  in 
different  cases,  and  depends  upon: — (i)  The  thickness  and 
character  of  the  media  (tissues  of  the  chest  wall,  lung,  etc.) 
which  separate  the  heart  from  the  hand  of  the  observer  ; 
(2)  The  force  with  which  the  heart  is  contracting. 

Diminution  or  absence  of  the  cardiac  impulse  (as  seen 
and  felt  over  the  prsecordial  region)  on  the  one  hand,  and 
excessive  impulse  on  the  other,  do  not,  therefore,  necessarily 
indicate  actual  diminution  or  actual  increase  of  the  cardiac 
contractions, — though  they  certainly  suggest  these  conditions. 

Diminished  Cardiac  Impulse. 

We  will  first  consider  those  cases  in  which  the  cardiac 
impulse,  as  seen  by  the  eye  and  felt  by  the  hand,  is  weakened 
or  abolished.  In  these  cases,  as  I  have  just  stated,  the  force 
of  the  cardiac  contraction  is  sometimes  apparently,  sometimes 
actually,  weakened. 

The  conditions  ivhich  give  rise  to  diminution  or  absence  of  t/ie 
cardiac    impulse,    the  force    of  the    cardiac    contractions 
being  normal  (i.e.  to  apparent  diminution  of  the  force  of 
the  cardiac  contractions),  are  as  follozus  : — 
I.   Undue  thickness  of  the  thoracic  walls,  especially  the 
presence  of  a  thick  layer  of  subcutaneous   fat,  largely  de- 
veloped mammae,  etc.^ 

'  In  these  cases  (where  the  subcutaneous  fat  is  excessive)  the  heart  may  be 
infiltrated  with  fat,  or  in  a  condition  of  true  fatty  degeneration,  and  the  force  of 
the  cardiac  contractions  may  be  actually  as  well  as  apparently  diminished. 


1 1 8  Diseases  of  tJie  Heart. 

2.  Excessive  over-lapping  of  the  heart  by  the  lungs. 
This  condition  is  seen  even  in  health  where  the  thorax  is 
unusually  short  and  broad,  and  the  lungs  voluminous  ;  but  it 
reaches  its  highest  degree  of  development  in  pulmonary 
emphysema. 

3.  Fluid  in  the  sac  of  the  pericardium.  When  the 
effusion  is  scanty,  the  position  and  force  of  the  apex  beat 
may  not  be  altered.  When  the  effusion  is  more  considerable, 
the  apex  is  raised  and  carried  more  to  the  left,  and  the 
cardiac  impulse  as  felt  by  the  hand  is  weakened.^  When 
the  effusion  is  very  great,  the  apex  beat  may  completely 
disappear,^  and  it  may  be  impossible,  when  the  patient  is 
lying  on  his  back,"^  to  feel  any  cardiac  impulse. 

The  conditions  ivliich  give  rise  to  actual  dimiiuition  of  the  force 
of  the  cardiac  contractions,  and  therefore  of  the  cardiac 
impulse,  as  felt  by  the  hand  externally,  are : — 

1.  General  collapse,  and  anything  which  temporarily 
weakens  the  action  of  the  heart — (nervous  depression,  exces- 
sive smoking,  etc). 

2.  Structural  alterations  which  weaken  the  cardiac  muscle, 
such  as  fatty  degeneration,  fibroid  degeneration,  acute  myo- 
carditis, etc. 

Increased  Cardiac  Impulse. 

Increased  cardiac  impulse,  as  seen  and  felt  over  the  prsc- 
cordia,  like  diminished  impulse,  may  be  either  apparent  or 
real. 

The  conditions  zuhich  gives  rise  to  increased  cardiac  impnlsc — 
tlie  force  of  the  cardiac  contractions  remaining  normal — 
{apparent  increase^  are  as  follows : — 
I.  An  atrophied  condition  of  the  chest  walls.     This  cause 

'  In  some  of  these  cases  the  visible  impulse  may  be  considerable,  but  the 
impulse,  as  felt  by  the  hand,  slight. 

-  In  many  cases  of  excessive  pericardial  effusion,  the  force  of  the  cardiac  con- 
tractions is  also  actually  impaired. 

'  The  cardiac  impulse  can  generally  be  felt  if  the  patient  is  made  to  lean 
well  forwards,  or  turn  on  to  his  left  side. 


The  rhythm  and  celerity  of  the  cardiac  impulse.  1 19 

is,  to  a  large  extent,  theoretical  and  of  little  importance  in 
practice.  Atrophy  of  the  subcutaneous  fat,  and  of  the  chest 
muscles  (the  lungs  being  normal),  probably  exerts  little 
influence  on  the  cardiac  impulse  as  felt  externally.  Indeed 
in  many  of  these  cases  the  heart  is  itself  debilitated,  and  as 
a  matter  of  fact  the  impulse  weakened. 

2.  Increased  exposure  of  the  heart.  This  is  a  frequent 
cause  of  increased  pulsation,  and  is  usually  due  to  the 
retraction  of  the  lungs,  which  results  from  pleurisy,  cirrhosis, 
etc. ;  but  it  may  be  due  to  forward  displacement  of  the  organ. 

TJic  conditions  ivJiich  produce  actual  increase  of  the  force  of 
t/ic  cardiac  contractions,  and  therefore  of  the  cardiac  inipidse,  as 
seen  and  felt  externally,  are  : — 

1.  All  conditions  which  produce  temporary  over-action  of 
the  heart,  such  as  violent  exertion,  mental  agitation,  and  the 
numerous  causes  of  functional  palpitation. 

2.  Hypertrophy  of  the  heart ;  particularly  hypertrophy  of 
the  left  ventricle.  In  these  cases  the  cardiac  impulse  is 
heaving  or  pushing,  and  the  whole  chest  may  appear  to  be 
raised  en  masse. 

The  Rhythm  of  the  Cardiac  Contractions. 

When  the  cardiac  impulse  is  perceptible,  the  exact  rhythm 
of  the  cardiac  contractions  can  of  course  be  ascertained  by 
palpating  the  prascordia,  but  the  rhythm  of  the  heart  will 
be  more  appropriately  considered  when  I  come  to  treat  of 
the  pulse. 

The  Celerity  of  the  Cardiac  Impulse. 

In  some  conditions,  the  heart  contracts  more  abruptly 
than  in  health,  and  the  impulse,  as  seen  and  felt  externally, 
is  correspondingly  sudden.  This  form  of  impulse  (due  to 
increased  celerity  of  contraction)  is  chiefly  seen  in  conditions 
of  nervous  excitement,  and  of  '  irritable  weakness,'  such  as  is 
associated  with  anaemia  and  allied  conditions.  The  area  of 
visible  impulse  is  often  increased. 

In  other  cases  the  cardiac  contraction,  and  therefore  the 


I  20  Diseases  of  fJic  Heart. 

impulse  as  seen  and  felt  externally,  are  unusually  slow  and 
laboured  (diminished  celerity  of  impulse).  This  form  of 
contraction  is  generally  associated  with  hypertrophy,  more 
especially  hypertrophy  of  the  left  ventricle  ;  the  cardiac 
impulse  is  usually  strong  and  pushing,  and  in  many  cases 
the  chest  appears  to  be  raised  up  en  masse. 

Proicordiai  thrills  and  friction  fremitus. 

Vibratile  sensations,  of  a  '  soft '  trembling  character,  and 
resembling  very  closely  the  vibratile  sensation  which  is  ex- 
perienced on  placing  the  hand  over  the  back  of  a  cat,  when 
purring  (hence  the  term  '  purring  tremor '  which  has  been 
applied  to  them),  are  sometimes  felt  on  placing  the  hand  over 
the  praecordia.  To  vibrations  of  this  description  the  term 
thrill  is  applied.  The  term  friction  fremitus  is  given  to 
vibrations  of  a  harsher,  rougher,  and  grating  character,  which 
can  be  felt  when  the  hand  is  placed  over  the  chest. 

Thrills  may  be  produced  either  in  the  heart  itself  or  in 
the  great  vessels.  The  cardiac  thrills  with  which  we  are  now 
concerned,  are  usually  produced  by  the  passage  of  the  blood 
stream  through  a  stenosed  or  roughened  orifice,  and  are 
therefore  generally  produced  by  a  'direct'  current. 

Stenosis  of  the  mitral  valve  is  the  most  common  cause  of 
cardiac  thrill.  The  vibratile  sensation  is  felt  in  the  mitral 
area,  i.e.  over  the  position  of  the  apex  beat ;  its  rhythm  is 
(for  tlie  reasons  which  I  shall  afterwards  explain  in  speaking 
of  cardiac  murmurs)  presystolic,  that  is  to  say,  it  occurs 
immediately  before  the  contraction  of  the  ventricle,  i.e. 
immediately  before  the  apex  beat.  Aortic  stenosis  is  the 
next  most  common  cause  of  thrill.  The  vibratile  sensation 
is  systolic  in  rhythm,  and  is  felt  over  the  base  of  the  heart 
and  ascending  thoracic  aorta. 

Occasionally,  however,  the  thrill  is  produced  by  a  back- 
ward or  regurgitant  current.  A  systolic  thrill  over  the  apex 
is  felt  in  some  cases  of  mitral  regurgitation  ;  and  a  diastolic 
thrill  at  the  base  is  not  at  all  uncommon  in  aortic  regurgi- 
tation. Thrills  produced  at  the  tricuspid  and  pulmonary 
orifices  are  extremely  rare. 


Percussion.  121 

Friction  fremitus  is  produced  by  the  rubbing  together  of 
two  rough  surfaces.  When  felt  over  the  praecordia,  it  may  be 
pericardial  or  pleural. 

Pericardial  friction  fremitus  corresponds  in  rhythm  to 
the  rhythm  of  the  heart.  It  is  a  comparatively  rare  pheno- 
menon which  is  seen  in  some  cases  of  pericarditis,  more 
especially  in  those  cases  in  which  the  lymph  coating  of  the 
pericardial  sac  is  tough.  Pericardial  friction  fremitus  is 
therefore  observed  towards  the  later  periods  of  pericardial 
inflammation,  i.e.  when  the  lymph  is  becoming  tough  and 
organised.  The  clinical  signiiicance  of  pericardial  fremitus 
is  not  great,  for  friction  vibrations  are  almost  always  more 
apparent  to  the  ear  than  to  the  touch,  and  are  therefore 
better  studied  by  auscultation  than  by  palpation. 

Pleural  friction  is  sometimes  felt  over  the  praecordial 
region,  more  especially  over  the  borders  of  the  heart.  Its 
rhythm  corresponds  to  the  rhythm  of  the  respirations,  and  by 
this  means  it  is  distinguished  from  the  friction  fremitus  of 
pericarditis. 

PERCUSSION. 

Percussion,  the  next  method  of  physicial  examination 
which  we  employ,  is  an  extremely  important  means  of  in- 
vestigation. It  is  founded  on  the  facts: — (i)  that  the  heart 
is  a  solid  organ  which  is  in  great  part  surrounded  by 
the  air-containing  lungs  ;  and  (2)  that  the  '  sound '  and 
'  sensation  of  resistance,'  which  are  obtained  by  percussing 
a  solid  body  and  an  air-containing  viscus,  are  markedly 
different. 

The  object  of  percussion  is  to  ascertain  the  size,  the 
shape,  and  position  of  the  heart ;  and  in  order  to  determine 
these  points  we  must  endeavour  to  define: — (i)  the  extent 
and  outline  of  that  part  of  the  heart  which  is  uncovered  by 
lung, — the  area  of  superficial  or  absolute  cardiac  dulness ; 
(2)  the  size  and  outline  of  the  heart  as  a  whole — tJie  area 
of  deep  or  relative  dulness,  as  it  is  sometimes  termed — (the 
area  of  impaired  percussion). 


I  2  2  Diseases  of  the  Heart. 

The  area  of  superficial  or  absolute  eeirdiae  dulncss. 

The  size  of  the  area  of  superficial  or  absolute  cardiac  dulness 
varies  considerably,  in  health,  with  the  condition  of  the  lungs, 
being  diminished  during  inspiration,  and  increased  during 
expiration,  and  is  subject  to  marked  alterations  in  disease. 

Theoretically,  it  should  exactly  correspond  to  that  portion 
of  the  heart  which  is  uncovered  by  lung  (see  fig.  33),  but  as 
a  matter  of  fact  its  inner  (central)  border  does  not  correspond 
to  the  mid-line  of  the  sternum,  but  to  the  left  border  of  that 
bone  ;^  while  its  inferior  border  cannot  be  accurately  deter- 
mined by  means  of  percussion.^ 

The  extent  of  the  heart,  which  is  uncovered  by  king,  during  moderate 
inspiration,  is  seen  in  figure  ■}^'}^.  In  full  inspiration,  the  anterior  border  of 
the  right  lung  closely  corresponds  to  a  line  drawn  vertically  downwards 
through  the  centre  of  the  sternum.  It  extends  downwards  as  far  as  the 
junction  of  the  sixth  costal  cartilage  with  the  sternum  ;  the  lower  border 
of  the  lung  leaves  the  middle  line  usually  at  the  level  of  the  sixth  rib  or 
sixth  interspace,  and  passes  obliquely  downwards  and  backwards. 

The  anterior  border  of  the  left  lung  closely  corresponds  to  the  mid- 
line of  the  sternum  until  it  reaches  the  level  of  the  fourth  costal  cartilage. 
At  this  point  it  passes  obliquely  downwards  and  outwards  until  it  reaches 
a  point  which  usually  corresponds  to  the  junction  of  the  fifth  rib  with 
its  costal  cartilage.  It  then  turns  obliquely  inwards  and  downwards, 
forms  the  tongue-shaped  projection,  which  is  well  shown  in  the  figure,  and 
finally  passes  backwards  and  downwards,  usually  leaving  the  middle  line 
at  the  level  of  the  sixth  rib  or  sixth  inter-space. 

The  area  of  superficial  or  absolute  cardiac  dulness  is,  then, 
more  or  less  triangular^  in  shape;  the  size  of  the  triangle 
varying  with  the  position  of  the  anterior  borders  of  the 
lungs. 

'  The  sternum  is  an  excellent  conductor  of  sound,  and  it  is  difficult  or  impos- 
sible when  one  lateral  half  is  in  contact  with  the  resonant  lung,  as  it  is  during 
complete  inspiration,  to  get  an  absolutely  dull  percussion  sound  over  the  other 
(the  right)  half  of  the  bone. 

^  The  lower  border  of  the  heart  cannot  be  accurately  defined  by  percussion,  for 
it  is  practically  impossible  to  distinguish  the  dull  sound  which  is  due  to  the  lower 
part  of  the  heart,  and  the  dull  sound  which  is  due  to  the  upper  part  of  the  liver. 

'  In  many  cases,  the  area  of  superficial  cardiac  dulness  is  rather  quadrangular 
than  triangular. 


Area  of  absolute  eardiac  d illness. 


12X 


The  base  of  the  triangle  cannot,  for  the  reason  ah-eady 
given  (see  foot-note,  page  122),  be  accurately  defined  by  per- 
cussion, but  is  represented  with  sufficient  accuracy  by  a 
horizontal  line  drawn  from  the  position  of  the  apex  beat  to 
the  mid-sternum.  Under  normal  circumstances,  and  during 
moderate  inspiration,  the  length  of  the  base  line  is  about  2\ 
inches. 


Fic.   33. — Snpe7-Jicial  view  of  the  organs  of  the  chest  and  abdomen  from  the  front, 
shoiV/n:;-  the  part  of  the  heart  uncovered  by  Ii(ng.      {Enlarged  from  Sibson. ) 


124 


Diseases  of  tJie  Heart. 


Fig.  34.  —  The  area  o/pnccordial  Jiilness  in  middle  ai;v.     (After  Weil.) 

ABCD,  area  of  superficial  or  absolute  cardiac  dulness  ;  AIK,  area  of  im- 
paired percussion  or  deep  dulness  ;  CE,  lower  border  of  right  lung  ;  DF,  lower 
border  of  left  lung;  G  and  H,  upper  borders  of  lungs  ;  PQ,  upper  border  of  hepatic 
dulness  ;  LM,  lower  border  of  hepatic  dulness  ;  NO,  lower  border  of  stomach  in 
n)oderate  distention. 


Area  of  absolute  cardiac  di  tin  ess.  125 

The  apex  of  the  triangle  corresponds  under  normal  cir- 
cumstances to  the  junction  of  the  fourth  left  costal  cartilage 
with  the  sternum. 

The  vertical  side  of  the  triangle,  i.e.  the  side  formed  by  a 
line  drawn  from  the  apex  of  the  triangle  to  the  central  (the 
sternal)  end  of  the  base  line,  is,  under  normal  circumstances, 
about  two  inches  in  length.  For  the  reason  already  given 
(see  foot-note,  page  122)  it  does  not  correspond  to  the  mid-line 
of  the  sternum,  but  to  the  left  border  of  the  bone. 

The  third  or  oblique  side  of  the  triangle,  which  is  seldom 
a  straight  line,  but  generally  more  or  less  curved,  as  repre- 
sented in  figures  34  and  35,  is  formed  by  drawing  a  line  from 
the  apex  of  the  triangle  to  the  outer  end  of  the  base-line 
{i.e.,  to  the  apex  of  the  heart)  ;  it  is  usually  about  3  inches 
in  length. 

Mode  of  percussiug  the  area  of  superficial  or  absolute 
cardiac  dulness.  In  seeking  to  determine  the  exact  size 
and  boundaries  of  the  area  of  superficial  or  absolute 
cardiac  dulness,  at  the  bedside,  it  is  convenient  in  the 
first  place,  as  recommended  by  Sansom,  to  draw  the 
base-line,  i.e.  to  draw  a  horizontal  line  from  the  position  of 
the  apex  beat  to  the  mid-sternum,  and  then  to  determine 
the  position  of  the  vertical  and  oblique  sides  of  the  triangle 
respectively,  i.e.  to  define  the  anterior  margins  of  the  lungs 
by  means  of  percussion.  And  it  is  important  to  remember 
that  at  those  points  at  which  the  absolute  and  relative 
areas  of  cardiac  dulness  meet  [i.e.  where  the  margins  of 
the  lungs  terminate),  the  percussion  strokes  must  be  lightly 
struck,  for  otherwise  the  resonant  note  which  is  obtained 
from  the  thin  layer  of  lung  will  be,  to  some  extent,  obscured 
by  the  dull  sound  which  is  obtained  from  the  solid  heart, 
which  is  situated  beneath  it.  The  extent  of  the  area  of 
absolute  cardiac  dulness,  both  in  moderate  inspiration,  and 
during  complete  inspiration,  and  in  complete  expiration, 
should  be  ascertained  if  extreme  accuracy  is  required,  per- 
cussion being  performed,  while  the  patient  holds  his  breath, 
after  a  moderate  inspiration,  a  complete  inspiration,  and  a 
complete  expiration,  respectively. 


126 


Diseases  of  tJie  Heart. 


Fig.  35. — Atitei-ior  view  of  the  chest  and  abdomen,  showing  the  position  of  the  heart 
in  the  thorax  and  its  relationship  to  the  surrounding  viscera.  (After  Weil. ) 
EF,  edge  of  the  right  king;  GH,  edge  of  the  left  lung;  MN,  right  border  of 
the  heart ;  NO,  lower  border  of  the  heart ;  PO,  left  border  of  the  heart ;  Q,  sinus 
mediastinocostalis,  situated  between  the  edge  of  the  pleura  and  incisura  cardiaca 
of  the  anterior  border  of  the  left  lung ;  R,  highest  point  of  the  portion  of  liver 
covered  by  lung;  S,  lower  edge  of  the  liver;  T,  cardiac  portion  of  the  stomach; 
U,  pyloric  portion  of  the  stomach  ;  V,  small  curvature  of  the  stomach  ;  \V,  greater 
curvature  of  the  stomach. 


TJie  area  of  deep  or  relative  cardiac  dulness.      127 

TJie  area  of  deep  or  relative  cardiac  dnlitcss. 

The  area  of  deep  or  relative  cardiac  dulness  should  cor- 
respond to  the  space  which  the  heart  occupies  as  a  whole, 
that  is  to  say,  it  should  extend  vertically  from  the  third  rib 
or  second  interspace  to  the  base-line  drawn  from  the  apex 
beat  horizontally  across  the  sternum,  and  transversely  from 
an  inch  to  the  right  of  the  sternum  to  a  point  slightly  within 
the  left  nipple.  (See  fig.  35.)  As  a  matter  of  fact,  how^ever, 
it  is  difficult  to  define  the  exact  extent  of  the  deep  cardiac 
dulness.  As  we  have  already  seen,  its  lower  border  cannot 
be  accurately  ascertained  by  means  of  percussion.  Its  upper 
boundary  runs  into  the  dulness  which  is  due  to  the  presence 
of  the  great  vessels  (aorta,  pulmonary  artery,  and  superior 
cava,  etc.)  ;  while  the  right  and  left  borders  of  the  heart  (more 
particularly  the  right)  are  so  deeply  situated,  that  their  exact 
position  is  with  difficulty  determined. 

The  left  border  can  generally  be  fairly  well  defined, — and  we  have  an 
additional  guide  to  its  position  in  those  cases  in  which  the  apex  beat  is 
well-marked,  for  the  position  of  the  left  apex  beat  not  only  represents  the 
lowest,  but  also  the  outermost  point  of  the  heart.  (In  some  cases  of 
pericardial  effusion,  and  in  some  cases  of  hypertrophy  of  the  left  ventricle, 
the  cardiac  dulness  extends  farther  to  the  left  than  the  position  of  the 
apex  beat.)  When  the  right  ventricle  is  dilated,  the  left  apex  beat  may 
be  ill  defined  or  absent.  In  cases  of  this  description  the  pulsation  of  the 
right  ventricle  is  often  best  marked  in  the  epigastrium,  and  the  position 
of  the  apex  beat  affords  no  guide  to  the  left  border  of  the  heart. 

Mode  of  percussing  the  deep  cardiac  duluess.— The  observer 
should  first  endeavour  to  define  the  upper  border  of  the  heart 
by  percussing  from  above  downwards  in  the  para-sternal 
line.^  He  should  then  determine  the  extent  of  the  transverse 
dulness  at  the  level  of  the  fourth  rib  or  fourth  interspace. 
The  percussion  must  be  forcibly  made,  for  the  borders  of  the 
heart  are  covered  by  a  thick  layer  of  resonant  lung ;  small 
differences  in  tone  must  be  accurately  noted,  and  the  '  per- 
cussion resistance '  carefully  observed. 

'  The  para-sternal  line  is  an  imaginary  line  drawn  vertically  downwards  over 
the  front  of  the  chest  mid-way  between  the  left  border  of  the  sternum  and  the  left 
nipple. 


I  28  Diseases  of  the  Heart. 

Alterations  in  the  extent  of  the  cardiac  diilness  %:^hich  occur 
in  disease. 

The  area  of  cardiac  dulness  may  be  either  increased  or 
diminished  in  disease  ;  and  both  conditions — increased  and 
diminished  duhiess  over  the  praecordia — may  be  either 
actually  or  apparently  due  to  cardiac  alterations.  In  other 
words,  alterations  in  the  extent  of  the  praecordial  dulness  are 
in  some  cases  due  to  alterations  in  the  size  of  the  heart  and 
pericardium  ;  in  other  cases,  to  alterations  in  the  surrounding 
viscera  (more  particularly  in  those  portions  of  the  lungs 
which  overlap  the  heart),  the  size  of  the  heart  and  peri- 
cardium being  normal. 

Increased  dulness  over  the  prcecordia. 
Increased  dulness  over  the  praecordia  may  be  due  to  : — 

1.  Increase  in  the  size  of  the  heart  (hypertrophy,  dilata- 
tion, deposits  of  fat  on  the  exterior  of  the  heart,  new  growths 
in  its  substances). 

2.  Fluid  in  the  sac  of  the  pericardium  (pericarditis  with 
effusion,  hydro-pericardium). 

3.  Increased  exposure  of  the  heart — the  organ  itself  being 
of  normal  size.     Under  this  head  are  included  : — 

(a)  Those  cases  in  which  the  anterior  borders  of  the  lungs 
are  retracted  from  pleuritic  adhesions,  cirrhosis,  etc. 

(b)  Those  rarecases  in  which  the  heart  is  displacedforwards 
by  aneurisms  or  solid  tumours  in  the  posterior  mediastinum. 

4.  Solid  or  fluid  accumulations  in  contact  with  the  heart, 
amongst  which  the  following  are  the  most  important : — 

(a)  Consolidations  (from  pulmonary  apoplexy,  pneumonia, 
tubercle,  new  growths,  etc.),  of  those  portions  of  the  lungs 
which  overlap  the  heart. 

(b)  Fluid  in  the  pleural  sacs. 

(c)  Solid  tumours,  deposits  of  fat,  or  inflammatory  forma- 
tions in  the  anterior  mediastinum. 

(d)  Enlargements  of  the  liver. 

(e)  Aneurisms  springing  from  the  base  of  the  aorta. 

Note. — It  is  extremely  important  to  remember  that  the  dulness  which, 
under  ordinaiy  circumstances,  results  from  enlargement  of  the  heart   and 


Increased  Prcecordial  D illness.  129 

many  of  the  other  conditions  which  I  have  enumerated  in  the  text,  may 
not  be  present  in  those  cases  : — in  which  the  lungs  are  emphysematous  ; 
in  which  the  anterior  margins  of  the  lungs  are  fixed  by  adhesions  ;  or  in 
which  there  is  air  in  the  pericardial  or  pleural  sacs. 

TJie  differential  diagnosis  of  increased  dulness  over  the 
prcecordia. 

Given  the  presence  of  increased  dulness  over  the  prae- 
cordia,  we  must,  of  course,  endeavour  to  determine  the  exact 
nature  of  the  pathological  condition  which  is  present ;  and  in 
order  to  arrive  at  this  conclusion,  it  is  convenient  to  proceed 
by  the  following  stages  or  steps  :  — 

Step  No.  I. — Is  the  increased  dulness  derived  from  the 
heart  itself,  or  is  it  due  to  the  presence  of  some  non-resonant 
substance  in  contact  with  the  organ  ? 

Step  No.  2. — If  the  dulness  is  due  to  the  presence  of  a 
non-resonant  substance  in  contact  with  the  heart,  what  is  the 
exact  pathological  condition  which  is  present  ? 

Step  No.  3. — If  the  dulness  is  directly  derived  from  the 
heart  itself,  does  it  result  from  increased  exposure  (apparent 
enlargement)  of  the  organ,  or  from  an  actual  increase  in  the 
size  of  the  heart,  including  the  pericardium  ? 

Step  No.  4. — If  the  dulness  is  due  to  an  actual  increase  in 
the  size  of  the  organ,  does  it  result  from  the  presence  of  fluid 
in  the  sac  of  the  pericardium,  or  from  an  enlargement  of  the 
heart  itself? 

Step  No.  5. — If  the  dulness  is  due  to  enlargement  of  the 
heart  itself,  is  the  enlargement  general  or  partial,  and  what  is 
the  pathological  character  and  cause  of  the  condition  ? 

Step  No.  I.— Is  the  increased  dulness  over  the  prcecordia 
derived  from  the  heart  itself,  or  is  it  due  to  the  presence  of  some 
iiflji-resojiant  substance  in  contact  ivith  the  organ  ? 

As  a  rule  there  is  little  difficulty  in  coming  to  a  correct 
conclusion  on  this  point.  As  we  have  previously  seen,  the 
chief  pathological  conditions  which  give  rise  to  dulness  in 
the  neighbourhood  of  the  heart,  are: — 

(a)  Consolidations  of  the  adjacent  portions  of  the  lungs 
(apoplectic,  pneumonic,  tubercular,  sarcomatous,  etc.). 

I 


I  30  Diseases  of  the  Heart. 

(b)  Fluid  in  the  pleural  cavity. 

(c)  Enlargement  of  the  liver. 

(d)  Tumours,  or  inflammatory  deposits  in  the  anterior 
mediastinum. 

(e)  Aneurism  of  the  first  portion  of  the  aortic  arch. 

Now  in  most  of  these  conditions — in  the  vast  majority 
of  cases  met  with  in  practice — the  increased  dulness  is  not 
confined  to  the  limits  of  the  praicordia,  but  extends  often 
for  a  considerable  distance  into  the  surrounding  regions  of 
the  chest.^  In  many  cases  too,  it  does  not  conform  to  the 
shape  of  the  dulness  which  results  from  an  enlargement  of 
the  heart  or  pericardium.- 

There  are,  too,  as  a  rule,  other  symptoms  and  physical 
signs  indicative  of  the  cause  of  the  dulness.  In  consolida- 
tions of  the  lung,  for  example,  cough,  expectoration,  and 
alterations  of  the  respiratory  murmur  over  the  seat  of  the 
dulness  (tubular  breathing,  rales,  etc.),  would  probably  be 
present. 

In  addition  to  these  positive  facts  the  negative  evidence — 
that  there  are  no  signs  nor  symptoms  of  disease  of  the 
heart  or  pericardium — confirms  the  diagnosis. 

The  points,  then,  to  which  attention  should  be  directed,  in 
order  to  come  to  a  conclusion  as  to  the  first  step  in  the 
diagnosis  are : — 

1.  The  extenfand  outline  of  the  dulness. 

2.  The  presence  of  symptoms  or  physical  signs  indicative 
of  disease  of  the  adjacent  parts. 

3.  The  condition  of  the  heart  and  pericardium,  as  deter- 
mined by  other  methods  of  investigation. 

Step  No.  2. — If  the  dulness  is  due  to  tJie presence  of  a  non- 

'  Dulness,  resulting  from  a  limited  consolidation  of  those  portions  of  the  lungs 
in  contact  with  the  heart,  might  of  course  be  limited  to  the  praacordia.  In  such  a 
case  the  other  physical  signs  and  symptoms  (negative  and  positive)  would  be  quite 
sufficient  to  determine  the  diagnosis. 

^  It  would  be  extremely  difficult,  indeed  in  many  cases  impossible,  to  dis- 
tinguish the  dulness  due  to  a  small  tumour  or  inflammatory  accumulation  in  the 
anterior  mediastinum,  from  the  dulness  which  results  from  enlargement  of  the 
heart  or  pericardium.  Fortunately  limited  tumours  of  this  description  are  rare, 
and  the  difficulty  in  diagnosis  is  therefore  seldom  met  with  in  practice. 


Increased  PrcFCordial  Dtilncss.  1 3 1 

resonant  substance  in  contact  ivith  the  heart,  i^'hat  is  the  exact 
pathological  condition  zv/iich  is  present  F 

This  point  can  only  be  determined  by  a  careful  and 
accurate  survey  of  all  the  'facts  of  the  case'  (symptoms, 
physical  signs,  etc.)  ;  and  it  would  obviously  be  out  of  place 
to  attempt  to  detail  here  the  numerous  symptoms  and 
physical  signs  which  characterise  the  many  different  condi- 
tions which  may  produce  dulness  in  the  neighbourhood  of 
the  heart.  Suffice  it  to  say,  that  the  observer  must  first 
endeavour  to  determine  to  which  group  of  conditions  (con- 
solidation of  the  lung,  fluid  in  the  pleura,  etc.),  the  lesion  is 
to  be  referred  ;  and  having  decided  that  point,  he  must  next 
endeavour  to  determine  the  exact  pathological  character  of 
the  structural  alteration  which  is  present. 

Step  No.  3. — If  the  dnlness  is  directly  derived  from  the  heart 
itself,  does  it  result  from  increased  exposure  (i.e.  apparent 
enlargement),  or  from  aetiial  increase  in  the  size  of  the  organ  ? 

By  far  the  most  common  cause  of  '  increased  exposure'  of 
the  heart  is  retraction  of  the  anterior  margins  of  the  lungs,  a 
condition  which  usually  results  from  pleurisy  or  cirrhosis. 

In  seeking  then  to  decide  whether  the  increased  dulness 
is  due  to  apparent  or  actual  enlargement  of  the  organ, 
attention  must  be  particularly  directed  to  the  condition  of 
the  lungs.  A  history  of  previous  pleurisy  ;  the  fact  that  the 
anterior  margins  of  the  lungs  are  fixed  by  adhesions,  and  do 
not  expand  and  cover  up  the  heart  during  inspiration — a 
point  which  can  be  determined  by  percussion  and  ausculta- 
tion, during  inspiration  and  expiration  respectively  ;  or,  the 
presence  of  symptoms  and  signs  of  cirrhosis,  phthisis,  etc., 
would  of  course  be  in  favour  of  increased  exposure  (apparent 
enlargement) — an  opinion  which  would  be  confirmed  by  the 
absence  of  symptoms  and  signs  of  pericardial  or  cardiac 
disease,  or  of  any  extra-cardiac  cause  of  enlargement  of  the 
heart,  such  as  cirrhosis  of  the  kidney  or  atheroma. 

But  while  these  are  the  points  to  which  attention  should 
be  directed,  in  order  to  make  a  diagnosis,  it  must  be  con- 
fessed that  a  positive  opinion  cannot  always  be  arrived  at ; 
and  it  is  still  more  difficult  to  exclude  any  enlargement  of 


132  Diseases  of  t lie  Heart. 

the  heart  itself,  in  those  cases  in  which  the  increased  exposure 
is  due  to  forward  displacement  of  the  organ.  In  many  of 
these  cases  the  heart  is  actually  enlarged  as  well  as  dis- 
placed ;  and  in  those  cases  in  which  there  is  no  enlargement 
of  the  organ,  the  strong  cardiac  impulse  which  may  be  very 
noticeable,  and  the  presence  of  intra-cardiac  murmurs,  which 
may  be  produced  by  pressure  alterations  at  the  valvular 
orifices,  may  make  it  impossible  to  exclude  all  cardiac 
hypertrophy.  In  cases  of  this  description  then  (which,  as  I 
have  previously  remarked,  are  extremely  rare),  a  positive 
opinion  that  the  increased  dulness  is  due  to  forward  dis- 
placement, and  not  to  enlargement  of  the  heart  itself,  could 
only  be  ventured  upon,  when  : — 

(a)  There  is  distinct  evidence  of  an  aneurism  or  tumour 
behind  the  heart,  i.e.  of  the  presence  of  an  efficient  cause  of 
forward  displacement. 

(b)  There  are  no  signs  nor  symptoms  of  cardiac  disease  ; 
and  no  extra-cardiac  cause  of  enlargement  such  as  chronic 
Bright's  disease. 

Step  No.  4. — If  the  dulness  is  due  to  an  actual  increase  in 
the  size  of  the  organ,  does  it  result  from  fluid  in  the  sac  of  the 
pericardium,  or  from  enlargement  of  the  heart  itself? 

This  question,  which  involves  the  differential  diagnosis  of 
pericardial  effusion  and  hypertrophy  and  dilatation  of  the 
heart,  will  be  more  appropriately  considered  in  the  detailed 
description  of  pericarditis,  which  will  be  afterwards  given. 

Step  No.  5. — If  the  increased  dulness  is  due  to  enlargement 
of  the  heart  itself  is  the  enlargement  general  or  partial,  and 
zvhat  is  the  pathological  character  and  cause  of  the  condition  ? 

This  point,  too,  will  be  more  conveniently  considered 
under  the  detailed  description  of  hypertrophy  and  dilatation 
of  the  heart. 

DIMINISHED   DULNESS   OVER   THE   PRyECORDIA. 

Diminished  dulness  over  the  praecordia  is  comparatively 
seldom  due  to  diminution  in  the  size  of  the  heart  itself;  it 
most  frequently  depends  upon  some  alteration  in  the  lungs 
or  adjacent  viscera.     The  chief  causes  of  diminished  dulness 


Dimmished  PrcECordial  Dulness. 


jj 


over    the    praecordia    are,    in    the    order    of    their    relative 
frequency,  as  follows  : — 

I.  Increased  covering  up  of  the  heart  by  the  lungs.  By 
far  the  most  common  cause  of  this  condition  is  emphysema, 
but  it  is  sometimes  due  to  the  anterior  margins  of  the  lungs 
being  fixed  over  the  heart  by  pleuritic  adhesions  ;  or  to  the 
fact,  that  the  heart  is  pushed  up  under  cover  of  the  lungs  by 
some  gaseous,  fluid  or  solid  accumulation  in  the  abdomen. 

In  some  healthy  persons,  in  whom  the  lungs  are  very  voluminous,  the 
area  of  absolute  cardiac  dulness  is  much  smaller  than  usual,  and  may  be 
completely  abolished  during  a  full  inspiration  ;  but  these  cases  are  easily 
recognised  by  the  facts,  that  the  area  of  cardiac  dulness  is  present  during 
a  full  expiration,  and  that  there  are  no  signs  nor  symptoms  of  cardiac  or 
pulmonary  disease. 

2.  Gaseous  accumulations  in  the  pleura,  stomach,  or 
intestines. 

3.  Gas  in  the  pericardium. 

4.  Atrophy  of  the  heart  itself 

TJie  dijfcrential  diagnosis  of  diminished  dulness  over  the 
prceeordia. 

There  is  not,  as  a  rule,  much  difficulty  in  deciding  this 
question.  The  steps  which  it  is  convenient  to  follow  in 
order  to  arrive  at  a  correct  conclusion  are  as  follows  : — 

Step  No.  I. — Does  the  diminished  praecordial  dulness 
depend  upon  extra-  or  intra-cardiac  ^  conditions  } 

Step  No.  2.  —  If  extra-cardiac,  is  the  diminished  dulness 
due  (a)  to  some  abnormal  condition  of  the  lungs  ;  (b)  to 
distention  of  the  stomach  and  intestines  ;  or  (c)  to  air  in 
the  pleural  cavity  (pneumo-thorax).'' 

The  observer  should  remember  that  atrophy  of  the  heart 
sufficiently  great  to  cause  diminished  praecordial  dulness  is 
extremely  rare,  and  could  only  be  diagnosed  by  the  method 
of  exclusion. - 

'  Under  the  head  of  intra-cardiac  conditions,  I  include  abnormal  conditions  of 
the  pericardium,  as  well  as  of  the  heart  itself. 

-  Atrophy  of  the  heart  is  met  with  in  many  wasting  affections,  more  particularly 
in  cancer  of  the  pylorus.  In  many  cases  of  this  kind  (wasting  diseases  with 
atrophy  of  the  heait)  the  lungs  are  emphysematous,  and  the  diminished  precordial 
dulness  is  partly' due  to  increased  overlapping  of  the  heart  by  the  lungs. 


134  Diseases  of  the  Heart. 

In  all  cases,  then,  in  which  diminished  pra^cordial  dulness 
is  met  with,  the  practitioner  should,  in  the  first  place,  make  a 
careful  physical  examination  of  the  patient,  paying  particular 
attention  to  the  condition  of  the  lungs,  stomach,  and  adjacent 
viscera.  By  this  means  he  will  be  able  to  determine  whether 
the  physical  signs  of  emphysema,  pneumo-thorax,  or  any  of 
the  other  extra-cardiac  causes  of  diminished  dulness  (which  I 
have  just  mentioned)  are  present. 

When  the  diminished  dulness  is  due  to  pneumo-peri- 
cardium,  the  physical  signs  of  that  condition — which  are  very 
definite,  and  which  I  shall  afterwards  describe — will  be  dis- 
covered in  the  course  of  the  examination. 

Should  the  result  of  this  examination  be  negative  {i.e. 
should  physical  examination  fail  to  elicit  any  cause  for  the 
condition),  he  will  have  to  ask  himself  whether  the  diminished 
dulness  is  due  to  a  voluminous  (but  not  emphysematous)  con- 
dition of  the  lungs,  or  whether  it  is  caused  by  atrophy  of  the 
heart  itself  The  condition  of  the  general  health  ;  the  state  of 
the  cardiac  dulness  during  a  full  expiration  ;  ^  and  particularly 
the  presence  of  any  well  recognised  cause  of  atrophy  of  the 
heart,  such  as  cancer  of  the  pylorus,  are  the  points  to  which 
attention  is  to  be  directed  in  order  to  decide  this  point. 

AUSCULTATION. 

Auscultation  is  an  extremely  important  means  of  phy- 
sical examination.     It  is  founded  upon  the  facts  : — 

(i)  That  during  each  cardiac  revolution  certain  sounds 
are  generated  within  the  heart. 

(2)  That  these  sounds  depend  upon  definite  physical 
conditions,  more  especially  upon  the  condition  of  the  valve- 
flaps,  and  the  manner  in  which  they  are  closed  and  stretched. 

(3)  That  modifications  in  these  physical  conditions  {i.e. 
alterations  in  the  valve-flaps,  and  in  the  manner  in  which 
they  are  closed  and  stretched)  are  attended  by  correspond- 
ing modifications  in  the  cardiac  sounds. 

'  When  the  kings  are  vohiminous,  hut  otherwise  healthy,  the  cardiac  duhiess 
becomes  distinctly  perceptible  during  a  complete  expiration.  In  atrophy  of  the 
heart,  a  full  expiration  does  not  produce  such  a  marked  effect. 


A  iiscultation.  1 3  5 

By  means,  then,  of  auscultation,  we  are  able  to  obtain 
valuable  information  as  to  the  condition  of  the  valvular 
apparatus  of  the  heart  ;  and  since  the  mode  of  closure  and 
stretching  of  the  mitral  and  tricuspid  valves  depends,  in 
great  part,  upon  the  condition  of  the  walls  of  the  left  and 
right  ventricles,  and  since  the  manner  in  which  the  aortic 
and  pulmonary  valves  are  closed  and  stretched  depends 
upon  the  condition  of  the  aortic  and  pulmonary  blood- 
pressures,  we  have  in  auscultation  a  valuable  means  of 
ascertaining  the  condition  of  the  cardiac  muscle,  and  of 
the  blood-pressure  in  the  aorta  and  pulmonary  artery 
respectively. 

Further,  by  means  of  auscultation  we  can  observe  the 
rhythm  of  the  heart,  and  the  exact  frequency  of  the  cardiac 
contractions.^  Auscultation,  too,  is  the  most  important  means 
which  we  possess  of  determining  the  presence  of  disease  in 
the  pericardial  sac. 

The  main  objects  of  auscultation  are  to  ascertain  : — 

1.  Whether  both  cardiac  sounds  are  audible  or  not. 

2.  The  character  of  the  cardiac  sounds,  whether  normal 
or  not. 

3.  If  abnormal,  the  exact  nature  of  the  modifications 
which  are  present. 

But  in  order  that  these  points  may  be  thoroughly  under- 
stood, and  that  the  significance  of  their  different  modifica- 
tions may  be  correctly  appreciated,  I  must  now  describe 
the  normal  character  of  the  cardiac  sounds,  their  mode  of 
production,  the  nature  of  the  alterations  which  they  undergo 
in  disease,  and  the  manner  in  which  these  modifications  are 
produced. 

The  iioi'jiial  Heart  So?iiids  and  their  mode  of  produetiou. 

During  the  period  which  elapses  between  the  commence- 
ment of  one  ventricular  contraction  and  the  commencement 

'  In  some  cases  in  which  the  heart  is  acting  quickly  and  feebly,  and  more 
especially  in  those  cases  in  which  some  of  the  cardiac  pulsations  fail  to  reach  the 
wrist,  auscultation  and  the  cardiograph  are  the  only  certain  means  of  ascertaining 
the  exact  frequency  of  the  cardiac  contractions. 


136  Diseases  of  the  Heart. 

of  the  ventricular  contraction  immediately  succeeding  it,  that 
is  to  say,  during  every  complete  cardiac  revolution  or  cycle, 
two  sounds  are  generated,  which  are  termed  respectively  the 
first  and  second  sounds  of  the  heart.  The  two  sounds  are 
separated  by  periods  of  silence,  or  pauses,  as  they  are  tech- 
nically termed  ;  and  the  whole  cardiac  cycle  is  therefore 
composed  of  four  separate  parts,  viz.: — 

1.  The  first  sound. 

2.  The  first  silence  or  pause. 

3.  The  second  sound. 

4.  The  second  silence  or  pause. 

The_/z/'i"/  sound  corresponds  in  time  to  the  contraction  of 
the  ventricles,  i.e.  its  rhythm  is  systolic ;  and  it  is  mainly 
produced  by  the  sudden  tension  of  the  auriculo-ventricular 
(mitral  and  tricuspid)  valve-segments  and  their  chordae 
tendirieae,  partly  by  the  contraction  of  the  muscular  walls  of 
the  ventricles.^ 

The  second  sound  follows  the  contraction  of  the  ventricles, 
i.e.  its  rhythm  is  diastolic ;  and  it  is  produced  by  the  closure, 
and,  more  especially,  by  the  sudden  tension  of  the  arterial 
(aortic  and  pulmonary)  valve-flaps. 

Now,  since  the  heart  is  a  double  organ,  four  sounds  are  in 
reality  generated  during  each  cardiac  cycle,  viz.,  two  first 
sounds,  produced  by  the  sudden  tension  of  the  mitral  and 
tricuspid  valve-flaps  (the  mitral  first  sound  and  the  tricuspid 
first  sounds  respectively),  and  two  second  sounds,  produced 
by  the  sudden  tension  of  the  aortic  and  pulmonary  valve- 
flaps  (the  aortic  and  ptdinonary  second  sounds  respectively). 
But  in  as  much  as  the  action  of  the  two  hearts  is,  under 
ordinary  circumstances,  perfectly  synchronous,  the  two  first 
sounds  are  synchronous,  and  the  two  second  sounds  are 
synchronous  ;  and  hence  a  single  first  sound  (which  is  made 
up  of  the  mitral  and  tricuspid  first  sounds),  and  a  single 
second  sound  (which  is  made  up  of  the  aortic  and  pulmonary 

'  The  tilting  of  the  apex  against  the  wall  of  the  chest,  the  sudden  tension 
of  the  walls  of  the  ventricles,  and  the  passage  of  the  blood  from  the  ventricles 
into  the  aorta  and  pulmonary  artery,  have  also  been  thought  to  aid  in  the  pro- 
duction of  the  first  sound  of  the  heart. 


Normal  Heart  Sounds. 


^Zl 


second  sounds)  are  heard  when   the  stethoscope   is   applied 
over  the  praecordia. 

TJie  relative  duration  of  the  cardiac  sounds  and  silences. 

Under  ordinary  circumstances,  i.e.,  when  the  heart  is 
healthy  and  the  pulse  of  normal  frequency,  each  cardiac 
sound,  and  each  silence,  has  a  definite  duration,  which,  for 
practical  purposes,  is  sufficiently  accurately  expressed  as 
follows  : — If  the  whole  cardiac  cycle  be  divided  into  ten 
equal  parts,  the  first  sound  will  occupy  four-tenths,  the  first 
silence  one-tenth,  the  second  sound  two-tenths,  and  the 
second  silence  three-tenths  of  the  whole.  This  measurement 
which  is  taken  from  Walshe  {Diseases  of  the  Heart,  page  48), 
is  a  good  working  division,  though  not  absolutely  accurate. 
According  to  Dr  Gibson  ^  the  average  absolute  duration  of 
each  phase  of  the  entire  cardiac  cycle  is  as  follows  : — 


Auricular  Systole.        Ventricular  Systole. 

■I  12  sec.  •368  sec. 


Ventricular  Diastole. 

•578  sec. 


Entire  Cycle. 

1*058  sec. 


This  division  of  the  cardiac  cycle  is  graphically  represented 
in  figures  t,6  and  37,  by  reference  to  which  the  exact 
relationship  of  the  cardiac  sounds  and  silences  will  be  more 
easily  appreciated. 


Fig.  36. — Diagrammatic  representation  of  the  cardiac  cycle. 

I  =  first  sound. 
2=second  sound. 
A=first  or  short  silence. 
B=second  or  long  silence. 


'  Journal  of  Anatoviy  and  Physiology,  vol.  xiv.  p.  237. 


i^.S 


Diseases  of  the  Heart. 


Fig.  37. — Diagrammatic  representation  of  the  cardiac  cycle.     (After  Gairdner, 
modified  by  Sharpey). 

TJic  cJiaractcristic  features  of  tJie  individual  cardiac  sounds. 

The  first  sound  is,  as  we  have  seen,  systolic,  and  lasts 
twice  as  long  as  the  second,  which  is  diastolic  ;  but  in  addi- 
tion to  these  differences  in  rhythm  and  duration,  the  two 
sounds  present  certain  other  distinctive  features.  The  first 
sound  is  dull,  muffled,  and  booming  in  character  ;  it  gives 
one  the  impression  of  being  produced  at  some  distance  from 
the  ear  ;  while  the  second  sound  is  sharp,  abrupt,  accentuated, 
and  superficial,  i.e.  it  appears  to  be  produced  close  to  the 
ear.  The  syllables  lupp  dupp  give  a  very  good  idea  of  the 
normal  characters  of  the  cardiac  sounds. 

The  characteristic  features  of  the  first  sound  are  best 
heard  at  the  apex  of  the  heart,  those  of  the  second  sound  at 
the  base. 

But  further,  the  first  sound  which  is  produced  in  the  left 
heart  {i.e.  the  mitral  first  sound)  is  longer  and  more  muffled 
than  the  tricuspid  first  sound  ;  while  the  aortic  second  is 
louder  and  more  accentuated  than  the  pulmonary. 

TJie  points  of  differential  niaxininni  intensity  of  the  in- 
dividual sounds. 

In  order  to  appreciate  these  differences,  i.e.  in  order  to 
hear  the  sounds  which  are  generated  at  any  one  of  the  four 


Position  of  tJie  Cardiac    Valves.  139 

valvular  orifices,  apart,  so  far  as  is  possible,  from  the  other 
three,  it  is  necessary  to  listen  at  certain  points  of  the  chest 
wall,  which  I  am  in  the  habit  of  terming  the  points  of 
dijfcrciitial  inaxinnnn  intensity  of  cardiac  sounds  and  nuirmnrs. 
The  position  of  the  points  is  as  follows  : — 

Mitral  sounds  are  best  differentiated  at  the  apex  of  the 
heart. 

Tricuspid  sounds  at  the  lower  end  of  the  sternum,  or 
rather  at  the  junction  of  the  lower  left  costal  cartilages  with 
the  sternum.  (Some  authorities  say  the  junction  of  the  right 
lower  costal  cartilages  with  the  sternum.) 

Aortic  sounds  at  the  second  right  costal  cartilage. 

Pulmonary  sounds  at  the  third  left  costal  cartilage. 

The  fact,  that  the  distinctive  characters  of  any  individual  sound  (mitral, 
tricuspid,  aortic,  and  pulmonary)  are  not  well  heard  if  the  stethoscope  is 
placed  over  the  exact  position  of  the  valve  at  which  that  sound  is 
generated,  is  owing  to  the  close  juxta-position  of  the  valves.  According 
to  Walshe  '  a  superficial  area  of  half  an  inch  square  will  include  a  portion 
of  all  the  four  sets  of  valves  in  situ;  an  area  of  about  one  quarter  of  an 
inch,  a  portion  of  all  except  the  tricuspid  ; '  while  Sibson  states  that  each 
of  the  higher  orifices  overlaps  in  position  the  orifice  immediately  below  it. 
'  Thus  the  pulmonic  orifice  at  its  lower  and  right  edge  is  situated  to  a 
slight  extent  in  front  of  the  upper  and  left  edge  of  the  aortic  orifice  ;  the 
right  posterior  or  lower  flap  of  the  aortic  valve  is  situated  in  front  of  the 
upper  third  or  two-fifths  of  the  mitral  orifice  ;  and  the  lower  two-thirds 
or  three-fourths  of  the  mitral'  orifice  are  behind  the  corresponding  upper 
portion  of  the  tricuspid  orifice.' — Russell  Reynold's  System  of  Medicine^ 
vol.  iv.  p.  86. 

The  exact  relatiojts/iip  of  the  valves  to  the  surface  of  the  c/icst  is, 
according  to  the  same  observers  (Walshe  and  Sibson),  as  follows  : — 

Pulmonary. — According  to  Walshe '  '  the  upper  or  free  edge  of  the 
pulmonary  valves  lies  horizontally,  and  in  the  mass  of  persons,  a  shade 
above  the  upper  edge  of  the  third  left  cartilage,  the  body  of  the  valve 
consequently  a  little  lower  than  this, — the  left  edge  of  the  sternum  having 
closely  the  same  width  of  the  vessel  on  both  sides.' 

Aortic. — The  aortic  valves,  according  to  Walshe,  lie  horizontally  a  very 
little  further  inwards,  and  lower  than  the  pulmonary,  corresponding  to  the 
union  of  the  third  left  cartilage  with  the  sternum. 

According  to  Sibson  the  upper  and  left  border  of  the  aortic  orifice, 
especially  during  the  diastole,  is  situated  behind  the  lower  portion  of 
the  third  cartilage  near  the  sternum  ;   and  its  lower  and  right  border, 

'  Diseases  of  the  Heart,  fourth  edition,  p.  6. 


140 


Diseases  of  the  Heart. 


especially  during  the  systole,  is  situated  behind  the  middle  line  of  the 
sternum,  on  a  level  with  the  upper  portion  of  the  fourth  cartilage. 

Mitral. — The  attached  edge  of  the  mitral  valve,  according  to  Walshe, 
lies  almost  horizontally  about  a  quarter  of  an  inch  lower  than  the  attached 
bases  of  the  aortic  valves,  very  slightly  further  inwards  than  these,  and 
deeper  within  the  chest  than  the  tricuspid  valve.  The  attached  border 
lies  on  the  level  of  the  union  of  the  third  cartilage  with  the  sternum, 
nearer,  as  a  rule,  the  upper  than  the  lower  border. 

According  to  Sibson  the  mitral  orifice  is  seated  behind  the  left  half  of 
the  sternum,  at  the  upper  two-thirds  of  the  lower  third  of  that  bone,  on  a 
level  with  the  fourth  cartilage,  the  fourth  space,  and  the  upper  portion  of 
the  fifth  cartilage. 

Tricuspid. — '  The  attached  edge  of  the  tricuspid,'  according  to  Walshe, 


Fig.  38. — Diagram  to  illustrate  the  position  of  the  valvular  orifices.     (After  Gee, 

slightly  modified. ) 

Note. — The  aortic  valve  is  a  little  too  low. 


Alterations  of  the  Heart  Sounds.  141 

'  slantingly  placed  across  the  sternum  from  above  downwards,  and  from 
left  to  right,  inclines  from  the  neighbourhood  of  the  sternal  edge  of  the 
third  left  interspace  nearly  to  the  sternal  end  of  the  fourth  right  inter- 
space, or  fifth  right  cartilage  ;'  while  Sibson  states  that  in  a  healthy  man 
with  a  well-formed  chest,  the  tricuspid  orifice  is  situated  behind  the  lower 
fourth  of  the  sternum  to  the  right  of  the  middle  line  of  that  bone,  its 
upper  border  being  on  a  level  with  the  lower  edge  of  the  fourth  cartilage, 
and  its  lower  border  being  behind  the  lower  end  of  the  sternum,  and  the 
articulation  to  it  of  the  right  sixth  cartilage. 

Mode  of  distingnisJung  the  tivo  sounds  of  iJie  heart.  —Under 
ordinary  circumstances  there  is  no  difficulty  in  distinguishing 
the  two  sounds  of  the  heart ;  but  in  some  cases  of  disease, 
more  particularly  when  the  heart  is  acting  quickly  and 
irregularly,  and  when  the  first  sound  is  short  and  valvular, 
it  may  be  very  difficult  to  say  which  is  the  first  and  which  is 
the  second  sound.  The  same  difficulty  is  also  experienced 
in  the  observation  of  some  cardiac  murmurs.  Now,  in  both 
cases,  attention  must  be  particularly  directed  to  the  rhythm 
of  the  sound  or  murmur,  and  to  its  point  of  differential 
maximum  intensity.  In  the  case  of  murmurs  the  direction 
of  propagation  is  also  of  importance,  as  I  shall  afterwards 
point  out. 

In  order  to  ascertain  the  exact  rhythm,  the  observer  should 
listen  over  the  prsecordia,  and,  at  the  same  time,  apply  the 
fingers  of  the  right  hand  over  the  position  of  the  apex  beat. 
When  the  apex  beat  is  not  available,  the  sound  should  be 
timed  by  the  carotid  pulse.  The  radial  pulse  is  not  suitable 
for  this  purpose,  owing  to  the  fact  that  an  appreciable  in- 
terval elapses  between  the  contraction  of  the  ventricle  and 
the  occurrence  of  the  pulse  at  the  wrist. 

Alterations  in  the  heart  sounds  ivhieh  occur  in  disease. 

The  alterations  of  the  heart  sounds  which  occur  in  disease 
are  either  simple  modifications  of  the  normal  sounds  {quanti- 
tative changes),  or  absolute  alterations  {qualitative  changes). 

The  quantitative  changes  include  : — 

I.  Alterations  in  the  loudness  or  intensity,  and  in  the 
duration  or  sound  characters  (tone  and  purity)  of  the  cardiac 
sounds. 


142  Diseases  of  tJie  Heart. 

2.  xA.lterations  in  the  position  of  the  points  of  differential 
maximum  intensity. 

3.  Reduph'cations. 

The  quaHtative  changes  embrace  the  various  forms  of 
endocardial  and  exocardial  murmurs. 

Alterations  in  loudness  or  intensity} 

The  intensity  or  loudness  of  the  cardiac  sounds  may  be 
increased  or  diminished  in  disease.  In  some  cases,  all  four 
sounds  (mitral,  tricuspid,  aortic,  and  pulmonary)  are  modi- 
fied ;  in  others,  the  sound  produced  at  one  valvular  orifice 
only  is  affected. 

But  although  alterations  in  intensity  are  common  in 
disease,  it  must  not  be  supposed  that  all  variations  of  this 
description  are  pathological.  On  the  contrary,  we  know  that 
the  loudness,  of  the  heart  sounds,  varies  in  different  in- 
dividuals, even  in  health,  and  in  the  same  (healthy)  in- 
dividual under  different  conditions  ;  and  that  it  is  extremely 
difficult  to  fix  upon  an  average  healthy  standard.  When  the 
alteration  (from  what  we  consider  the  average  healthy 
standard)  is  considerable,  when  it  is  permanent,  and  more 
especially  when  some  organic  disease  (either  of  the  heart 
or  other  organ)  capable  of  producing  it,  is  present,  there  is 
no  difficulty  in  deciding  that  the  alteration  is  pathological. 
Another  point  which  enables  us  to  distinguish  some  of  the 
pathological  alterations  is  this,  that  in  the  physiological 
variations  of  intensity  the  relative  degree  of  loudness  of  the 
different  heart  sounds  is  generally  preserved,  the  aortic  se- 
cond sound,  for  instance,  being  louder  than  the  pulmonary, 
the  mitral  than  the  tricuspid  ;  whereas  in  some  of  the  patho- 
logical variations  the  relative  intensity  of  the  sounds  derived 
from  the  right  and  left  hearts  is  perverted,  the  pulmonary 
being  louder  than  the  aortic,  the  tricuspid  than  the  mitral.- 

'  Alterations  in  the  loudness  or  intensity  of  the  heart  sounds  are  very  often 
associated  with  alterations  in  the  duration  and  sound  characters ;  but  for  con- 
venience of  description  it  is  better  to  consider  each  of  these  modifications  separately. 

^  In  many  pathological  alterations  the  relative  intensity  of  the  sounds  derived 
from  the  right  and  left  hearts  is,  of  course,  preserved. 


Increased  Loudness  of  Heart  Sounds.         143 

The  intensity  or  loudness  of  the  heart  sounds,  as  heard 
over  the prcecordia,  is  the  resultant  of  two  conditions,  viz.  :— 

(i)  The  amount  of  sound,  so  to  speak,  which  is  generated 
within  the  heart. 

(2)  The  facility  with  which  the  sound  generated  within 
the  heart  is  conducted  to  the  ear. 

Variations  in  the  intensity  or  loudness  of  the  heart 
sounds,  as  heard  over  the  preecordia,  may  therefore  be  due 
to  :— 

(i)  Alterations  in  production. 

(2)  Alterations  in  conduction. 
For  convenience  of  description  we   may    term   the    former 
actual  and  the  latter  apparent  alterations. 

Let  us  now  consider,  in  more  detail,  the  pathological  and 
clinical  conditions  which  are  associated  with  increase  and 
diminution  of  the  heart  sounds,  as  heard  over  the  praecordia, 
respectively. 

Increased  intensitj  or  loudness  of  the  heart  sounds  as  heard 
over  the  prcBcordia. 

Increased  intensity  or  loudness  of  the  heart  sounds,  as 
heard  over  the  prjecordia,  may,  as  I  have  previously  stated, 
be  either  apparent  or  real. 

Apparent  increase. — In  this  condition,  in  which  the  heart 
sounds,  are  louder  than  in  health,  a  normal  amount  of  sound, 
so  to  speak,  is  generated  within  the  heart,  and  the  increased 
intensity,  as  heard  over  the  praecordia,  is  due  to  the  con- 
ditions for  the  conduction  of  sound,  from  the  heart  to  the  ear, 
being  more  favourable  than  in  health. 

Now  the  pathological  and  clinical  conditions  which  favour 
increased  conduction  are  : — 

1.  Abnormal  thinness  of  the  chest  wall,  wasting  of  muscle, 
and  especially  of  the  subcutaneous  fat. 

2.  Increased  exposure  of  the  heart,  which,  as  we  have 
already  seen,  may  be  due  to  retraction  of  the  anterior  margins 
of  the  lungs  (cirrhosis,  pleurisy,  etc.),  or  to  forward  displace- 
ment of  the  heart. 


T44  Diseases  of  I  he  Heart. 

3.  Consolidation  of  the  portions  of  the  lungs  adjacent  to 
the  heart  (pneumonia,  phthisis,  etc.). 

4.  The  presence  of  a  cavity,  suitable  for  the  amplification 
of  sound,  i.e.  a  thin-walled  cavity  in  contact  with  the  heart 
on  the  one  hand  and  with  the  chest  wall  on  the  other.  The 
cavity  may  be  situated  in  the  lung  itself  (as  in  phthisis)  ; 
in  the  pleura  (as  in  pneumo-thorax)  ;  or,  it  may  be  a  dilated 
stomach. 

5.  Air  in  the  sac  of  the  pericardium  (pneumo-pericardium). 
In  the  latter  cases  (4  and  5)  the  heart  sounds  usually  have  a 
metallic  or  amphoric  character,  and  are  sometimes  auto- 
audible. 

Real  or  actual  increase. — In  this  condition  the  amount  of 
sound  which  is  generated  within  the  heart,  is  above  the 
normal  healthy  standard.^ 

Now,  since  the  chief  causes  of  the  normal  heart  sounds 
are  the  closure,  and  more  particularly  the  sudden  tension  of 
the  valvular  segments,  it  follows  that  anything  which  produces 
more  forcible  closure  and  more  sudden  tension  of  the  valvular 
segments  will  produce  an  actual  increase.  It  is  necessary  to 
add,  that  the  valvular  segments  must  be  healthy  ;  where  they 
are  rendered  rigid  and  incapable  of  vibrating,  the  cardiac 
sounds  may  be  feeble,  muffled,  and  impure,  although  the 
other  conditions  which  favour  the  increased  production  of 
sound  are  present. 

In  some  cases  all  the  valvular  segments  are  more  forcibly 
and  suddenly  stretched,  and  all  the  cardiac  sounds  are  con- 
sequently intensified.  Excited  action  of  the  heart,  such  as 
results  from  violent  muscular  effort,  neurotic  palpitation, 
ex-ophthalmic  goitre,  etc.,  is  the  most  common  cause  of 
this  condition  (i.e.  of  increased  intensity  of  all  the  heart 
sounds). 

In  other  cases,  and  these  are  by  far  the  most  important 
in  a  diagnostic  point  of  view,  one  of  the  cardiac  sounds  only 
is  exaggerated. 

'  \Yhen  the  conditions  for  conduction  are  unfavourable,  the  heart  sounds, 
as  heard  over  the  pracordia,  may  be  of  normal,  or  even  diminished  intensity,  even 
although  the  amount  of  sound  generated  within  the  heart  is  in  excess. 


Accentuation  of  tJic  Aortic  Second  Sonnet.       145 

Increased  intensity  of  tJie  aortic  second  sound  occurs  in 
all  conditions  in  which  the  blood  pressure,  in  the  aorta, 
is  above  the  normal  (the  aortic  segments  must,  as  I  have 
previously  remarked,  be  fairly  healthy).  Increased  aortic 
tension  may  result  from  : — (a)  an  obstruction  to  the  pas- 
sage of  blood  through  the  arterial  system,  the  amount  of 
blood  propelled  into  the  arterial  system  (or  what  amounts 
to  the  same  thing,  the  force  of  the  cardiac  pump)  being 
normal ;  (b)  an  excessive  quantity  of  blood  being  pumped 
into  the  aorta,  the  peripheral  resistance  being  normal.  (When 
the  flow  through  the  peripheral  parts  of  the  circulation  is 
abnormally  free,  an  excessive  quantity  of  blood  may  be 
propelled  into  the  arterial  system  without  any  increase  of  the 
arterial  tension  resulting). 

The  chief  pathological  and  clinical  conditions,  therefore, 
associated  with  accentuation  of  the  aortic  second  sound  are  : — 

1.  Obstruction  to  the  passage  of  the  blood  through  the 
minute  arteries — a  condition  which  occurs  more  particularly 
in  chronic  Bright's  disease  (the  cirrhotic  form  of  kidney)  and 
in  atheroma.  (Dr  Broadbent,  Dr  Mahomed,  and  others  think 
that  the  chief  cause  of  the  obstruction  in  many  of  these  cases 
is  situated  in  the  capillary  system  of  vessels  rather  than  in 
the  minute  arteries.^) 

In  these  cases  the  left  ventricle  is  hypertrophied,  and 
there  is  therefore  a  double  cause  for  the  increased  aortic 
tension,  viz.,  obstruction  in  front,  and  the  powerful  propelling 
force  behind. 

2.  Atheroma,  dilatation,  and  aneurism  of  the  aorta. 

3.  Hypertrophy  of  the  left  ventricle. 

All  cases  of  hypertrophy  of  the  left  ventricle  are  not  attended  with  an 
accentuated  aortic  second  sound.  In  mitral  regurgitation,  for  example, 
there  is  usually  hypertrophy  of  the  left  ventricle,  but  in  consequence  of 
the  leak  through  the  mitral  orifice,  the  amount  of  blood  pumped  into  the 

1  aorta  (by  the  hypertrophied  left  ventricle)  is  usually  smaller  than  normal, 
the  aortic  tension  is,  therefore,  diminished,  and  the  aortic  second  sound 

j    decreased.     Again,  in  aortic  regurgitation,  although   the  hypertrophied 

I  and  dilated  left  ventricle  propels  an  excessive  amount  of  blood  into  the 
aorta,  the   aortic   second   sound    is,  in  consequence  of  the  incompetent 

i  '  British  Medical  Jonnial^  Aug.  25,  18S3,  p.  357. 

K 


146  Diseases  of  the  Heart. 

condition  of  llie  aortic  \alve  and  the  altered  condition  of  the  aortic 
segments,  usually  completely  absent,  and  replaced  by  a  murmur. 

Increased  intensity  of  the  pulmonary  second  sound. — In- 
creased intensity  of  the  pulmonary  second  sound  occurs  in 
all  those  conditions  in  which  the  blood-pressure  within  the 
pulmonary  artery  is  in  excess.  And  increased  pulmonary 
tension,  may,  like  increased  aortic  tension,  be  due  either  to 
obstruction  in  front,  or  increased  pressure  from  behind,  these 
two  causes  being  very  generally  combined. 

The  chief  clinical  conditions  associated  with  accentuation 
of  the  pulmonary  second  sound  are  : — 

1.  Mitral  lesions  (both  stenosis  and  regurgitation)  which 
produce  stagnation  of  the  blood  in  the  lungs. 

Skoda  was  the  first  to  direct  attention  to  the  great  im- 
portance of  the  accentuation  of  the  pulmonary  second  sound 
in  cases  of  mitral  stenosis,  and  to  point  out  that  the  'amount 
of  accentuation '  is  an  index  or  gauge  of  the  extent  of  the 
mitral  lesion.  It  must,  however,  be  remembered: — (i)  that 
this  statement  only  holds  good  so  long  as  the  right  ventricle  is 
powerful  and  the  tricuspid  valve  sound.  In  advanced  stages 
of  mitral  disease  the  pulinonary  second  soimd  may  be  less 
loud  than  at  the  earlier  periods  of  the  case,  the  explanation 
being  either,  that  in  consequence  of  the  right  ventricle  having 
become  feeble,  or  the  tricuspid  valve  having  given  way,  less 
blood  is  being  injected  into  the  pulmonary  artery  ;  the  blood 
pressure,  therefore,  and  consequently  the  intensity  of  the 
pulmonary  second  sound,  are  less  than  at  the  earlier  stages 
of  the  case,  i.e.  before  the  tricuspid  began  to  leak  ;  (2)  that 
in  gauging  the  extent  of  a  mitral  lesion  by  the  loudness  of 
the  pulmonary  second  sound,  it  is  necessary  to  allow  for  pul- 
monary causes  of  accentuation. 

2.  Some  lung  affections,  notably  cirrhosis  and  emphysema, 
in  which  there  is  a  primary  ^  obstruction  to  the  passage  of  the 
blood  through  the  lungs. 

3.  Hypertrophy  of  the  right  ventricle.  As  I  have  pre- 
viously pointed  out,  hypertrophy  of  the  right  ventricle  is 
a  secondary  condition  which  results  from  some   obstruction 

Primary,  as  compared  with  the  secondary  cthf.XxwzXioxx,  which  is  due  to  mitral  lesions. 


Increased  intensity  of  the  Mitral  First  Sound.     147 

to  the  passage  of  the  blood  through  the  lungs.  In  cases  of 
this  description  there  is,  therefore,  a  double  cause  for  the 
increased  pulmonary  tension,  which  produces  the  accentua- 
tion of  the  pulmonary  second  sound,  viz.,  obstruction  in  front 
and  increased  pressure  behind. 

Increased  intensity  of  tlic  mitral  first  sound. — When  the 
mitral  first  sound  is  much  intensified,  its  duration  and  tone 
are  usually  at  the  same  time  modified  ;  it  is  shorter  than 
normal,  more  abrupt,  more  accentuated  ;  in  fact  it  loses  the 
distinguishing  characters  of  the  first  sound,  and  assumes  those 
of  the  second. 

A  combined  condition  of  hypertrophy  and  dilatation, 
together  with  an  irritable  condition  of  the  muscular  fibre, 
attended  by  increased  rapidity  (celerity)  of  contraction,  are 
the  conditions  which  more  particularly  favour  the  production 
of  this  form  of  modification. 

Temporary  over-action  of  the  heart  (palpitation,  etc.)  is 
also  a  common  cause  of  increased  loudness  of  the  mitral  first 
sound  ;  but  in  cases  of  this  description,  the  other  cardiac 
sounds  are  also  intensified.^ 

It  might  readily  be  supposed  that  hypertrophy  of  the  left 
ventricle  would  produce  increased  loudness  of  the  mitral  first 
sound.  Such,  however,  is  not  the  case ;  in  fact,  in  solid 
hypertrophy  of  the  left  .ventricle  {i.e.  hypertrophy  without 
dilatation),  even  when  the  segments  of  the  mitral  valve  are 
perfectly  healthy  and  elastic,  the  mitral  first  sound  is  usually 
weaker  (more  muffled)  than  in  health  (see  page  154,  where 
the  cause  of  the  muffling  is  explained).  This  fact  is,  I  think, 
a  strong  argument  in  support  of  the  valvular  as  against  the 
muscular  origin  of  the  first  sound. 

Increased  intensity  of  the  tricuspid  first  sound,  usually  de- 
pends upon  hypertrophy  and  dilatation  of  the  right  ventricle. 
The  same  remarks,  which  have  just  been  made  regarding 
accentuation  of  the  mitral  first  sound,  apply  here  ;  the  right 
being  substituted  for  the  left  ventricle,  and  the  tricuspid  for 
the  mitral  valve. 

'  The  mitral  segments  must,  for  the  reasons  previously  given  (see  page  144), 
be  fairly  healthy,  i.e.,  sufficiently  elastic  to  be  thrown  into  vibration. 


148  Diseases  of  the  Hear  I. 

The  differential  diagnosis  of  increased  intensity  of  tlic  heart 

sonnds. 

The  recognition  of  the  cause  of  the  increased  intensity  of 
the  heart  sounds  is  not,  as  a  rule,  a  matter  of  much  difficult3^ 
The  steps  in  the  inquiry  are  as  follows  : — 

Step.  No.  I.  Are  all  the  heart  sounds  intensified  ;  or,  is  the 
accentuation  limited  to  the  sound  produced  at  one  of  the 
valvular  orifices  ? 

Step.  No.  2.  If  all  the  sounds  are  intensified,  is  the  con- 
dition due  to  some  temporary  cause,  such  as  over-action  from 
excitement,  neurotic  palpitation,  and  the  like  ;  or,  is  it  asso- 
ciated with  structural  changes  in  the  heart  ? 

The  points  to  which  attention  is  to  be  directed  in  order 
to  solve  this  question  are  (a)  the  presence  of  any  obvious 
cause  of  temporary  over-action  or  excitement ;  (b)  the  con- 
dition of  the  heart  after  a  sufficient  time  has  elapsed  to  allow 
of  any  temporary  over-action  from  nervousness,  excitement, 
etc.,  to  have  subsided  ;  and  especially  (c)  the  presence  or 
absence  of  any  indications  of  organic  change  (such  as  in- 
creased dulness  on  percussion,  etc.)  in  the  heart  itself 

Step  N'o.  3.  If  the  accentuation  is  confined  to  the  sound 
produced  at  one  of  the  valvular  orifices,  what  is  its  cause  ? 

When  the  aortic  second  sound  .is  accentuated,  attention 
must  be  particularly  directed  to  the  condition  of  the  urine  ; 
the  state  of  the  superficial  vessels ;  the  presence  or  absence 
of  pressure  symptoms  within  the  thorax,  and  the  physical 
examination  of  the  aortic  arch  ;  for  renal  disease,  atheroma, 
and  aneurismal  dilatations  of  the  aorta,  are,  as  we  have 
previously  seen,  the  most  common  causes  of  this  condition, 
i.e.  accentuation  of  the  aortic  sound.  It  is  important  too,  to 
note  the  condition  of  the  left  ventricle  ;  for  hypertrophy  of 
the  left  ventricle  is  another  cause  of  increased  loudness  of  the 
aortic  second  sound. ^ 

'  The  hypertrophy  of  the  left  ventricle,  which  is  associated  with  accentuation  of 
the  aortic  second  sound,  is  usually  secondary  to  some  form  of  arterial  obstruction. 
Hypertrophy  due  to  mitral  and  aortic  valve  lesions  is  not  (for  the  reasons  previously 
given)  usually  attended  by  increased  intensity  of  the  aortic  second  sound, 


Diminished  intensity  of  the  Heart  Sounds.       149 

When  the  pulmonary  second  sound  is  accentuated,  at- 
tention must  be  particularly  directed  to  the  condition  of  the 
mitral  valve,  for  mitral  lesions  are  the  most  common  (cardiac) 
cause  of  the  condition.  Should  the  mitral  valve  be  healthy, 
the  lungs  ^  must  be  carefully  examined,  and  the  presence 
or  absence  of  hypertrophy  of  the  right  ventricle  must  be 
noted. 

When  the  mitral  or  tricuspid  first  sounds  are  intensified, 
the  condition  of  the  left  and  right  ventricles  must  be  particu- 
larly investigated,  and  the  causes  of  hypertrophy  and  dilata- 
tion looked  for. 

DiuiinisJied  intensity  or  loudness  of  tlie  /wart  sounds  as  Iieard 
over  the  pracordia. 

Diminished  intensity  or  loudness  of  the  heart  sounds,  as 
heard  over  the  praecordia,  may  be  either  apparent  or  real. 

Apparent  diminution. — In  this  condition,  in  which  the 
heart  sounds,  as  Iieard  over  the  prcecordia,  are  less  loud  than 
in  health,  a  natural  amount  of  sound,  so  to  speak,  is  generated 
within  the  heart,  and  the  diminution  is  due,  either  to  (a)  the 
conditions  for  conduction  being  less  favourable  than  in  the 
normal  state,  or  to  (b)  the  heart  sounds  being  obscured  by 
other  sounds  produced  within  the  chest,  e.g.  bronchitic  rales.- 

Now  the  chief  pathological  and  clinical  conditions  which 
interfere  with  conduction  are  : — 

1.  Excessive  thickness  of  the  chest-wall  more  particularly 
of  the  subcutaneous  fat. 

2.  Abnormal  over-lapping  of  the  heart  by  the  lungs — a 
condition  which  reaches  its  highest  degree  of  development  in 
pulmonary  emphysema. 

3.  Fluid  in  the  sac  of  the  pericardium. 

Actual    diminution. — In    this    condition    the   amount   of 


*  We  have  previously  seen  that  accentuation  of  the  puhnonary  second  sound  is 
almost  always  due  to  obstraction  to  the  flow  of  blood  through  the  lungs,  and  that 
this  condition  may  be  primary.,  i.e.  due  to  primary  alterations  in  the  lungs, 
cirrhosis,  emphysema,  etc.,  ox  secondary,  i.e.  the  result  of  mitral  lesions. 

^  In  these  cases  it  may  be  impossible  to  hear  the  heart  sounds  although  the 
conditions  for  conduction  are  favourable. 


1  50  Diseases  of  the  Heart. 

sound  which  is  generated  within  the  heart,  is  less  than 
normal.  The  diminution  may  be  due  to  the  following 
conditions  : — 

1.  Less  forcible  closure  of  the  valve-segments. 

2.  Less  sudden  closure  of  the  valve-segments. 

3.  Structural  alterations  in  the  valve-segments,  which 
produce  loss  of  elasticity,  or  interfere  with  vibration.^ 

In  some  cases,  all  the  heart  sounds  are  weakened.  In 
others,  the  sound  produced  at  one  of  the  valvular  orifices  only, 
is  affected. 

The  clinical  and  pathological  conditions  associated  with 
diminished  intensity  of  ^//the  cardiac  sounds  are  : — ■ 

1.  Feeble  action  of  the  heart  resulting  from  temporary 
conditions,  such  as  syncope,  and  the  structural  changes 
which  affect  the  cardiac  muscle  in  the  course  of  an  attack  of 
continued  fever,  notably  in  typhus. 

2.  Feeble  action  of  the  heart  resulting  from  permanent 
structural  changes,  such  as  fatty  and  fibroid  degeneration, 
great  dilatation  of  the  ventricular  cavities,  etc. 

The  conditions  which  produce  diminished  intensity  of  the 
individual  heart  sounds  are  as  follows  : — 

Diminished  intensity  of  the  aortic  second  sound. — Diminished 
blood-pressure  in  the  aorta  is  the  usual  cause  of  this  con- 
dition ;  but  it  may  result  from  rigidity  of  the  aortic  cusps.- 

The  following  pathological  and  clinical  conditions  are  the 
usual  causes  of  diminished  blood-pressure  within  the  aorta, 

'  In  many  of  these  cases  the  sound  is  impaired  or  replaced  l)y  a  murmur. 

■  Diminished  intensity  of  the  aortic  second  sound,  due  to  this  cause,  is  seldom 
observed.  It  probably  could  only  occur  in  those  cases  in  which  the  rigidity 
was  considerable  ;  and,  when  the  rigidity  of  the  cusps  is  great,  the  aortic  valve  is 
very  often  incompetent,  and  the  aortic  second  sound  replaced  by  a  murmur.  It 
must,  too,  be  remembered  that  forcible  tension  (distention)  of  the  base  of  the 
aorta  probably  also  takes  part  in  the  production  of  the  aortic  second  sound. 

It  is  important  too,  to  remember,  that  rigidity  of  the  aortic  segments  is  often 
associated  with  general  atheroma  and  dilatation  of  the  aortic  arch ;  and  that  in 
those  conditions  the  aortic  second  sound  instead  of  being  enfeebled  is  usually 
accentuated.  If  the  aortic  segments  and  base  of  the  aorta  were  so  rigid  as  to  be 
incapable  of  acting  as  good  sound  producers,  accentuation  would  not,  of  course, 
be  observed,  even  where  there  was  atheroma  and  dilatation  of  the  aortic  arch  ;  but 
such  a  degree  of  rigidity  is  uncommon. 


Diminished  intensity  of  the  Heart  Sonnds.       151 

and   hence    of    diminished    intensity    of    the    aortic    second 
sound  : — 

1.  All  structural  changes  which  impair  the  'driving' 
power  of  the  left  ventricle,  such  as  fatty  and  fibroid  dege- 
neration of  the  cardiac  muscle,  dilatation,  etc.  In  these  cases 
the  amount  of  blood  propelled  into  the  arterial  system  is 
insufficient  to  keep  it  properly  distended,  and  the  aortic 
blood-pressure  is  consequently  below  the  normal. 

2.  Mitral  lesions  (both  stenosis  and  incompetence.)  Here 
again  the  amount  of  blood  discharged  by  the  left  ventricle 
into  the  aorta  is  below  the  normal  quantity.^ 

Diminished  intensity  of  the  pntvionary  second  sound  may 
result  from  muscular  weakness  or  dilatation  of  the  right 
ventricle,  or  from  disease  of  the  tricuspid  orifice.  These 
conditions  are  almost  always  secondary  either  to  mitral 
lesions  or  to  primary  lung  aftections.  Diminished  intensity 
of  the  pulmonary  second  sound  is  seldom,  therefore,  primary. 

It  usually  happens  that  the  pulmonary  second  sound  is 
accentuated  in  the  earlier  periods  of  these  cases  ;  and  it  is  only 
after  the  secondary  dilatation  of  the  right  ventricle  has  be- 
come considerable,  or  after  the  tricuspid  valve  has  given  way, 
that  the  accentuation  disappears,  and  diminished  intensity  of 
the  pulmonary  second  sound  is  observed.- 

Diminished  intensity  of  tJie  mitral  first  sound. — Weakness 
of  the  wall  of  the  left  ventricle,  whether  temporary  or  perma- 
nent, is  a  fertile  source  of  diminished  intensity  of  the  mitral 
first  sound.  In  many  of  these  cases  the  wall  of  the  right 
ventricle  is  affected  in  the  same  manner,  and  the  sounds  of 
the  right  heart  are  also  weakened. 

The  condition  may  also  be  due  to  the  fact,  that  the  valve- 
segments  are  less  suddenly  stretched  than  in  health.  This  is 
probably  one  cause  of  the  'muffling'  of  the  first  sound  which 

'  We  have  previously  seen  that  the  pulmonary  second  sound  is  accentuated  in 
mitral  stenosis.  The  contrast,  therefore,  between  the  aortic  and  pulmonary  second 
sounds,  is  great,  and  is  due  to  a  double  cause,  viz.,  diminution  of  the  aortic  and 
increase  of  the  pulmonary. 

^  In  most  of  these  cases  the  diminished  intensity  is  only  relative  as  compared 
with  the  marked  accentuation  in  the  earlier  periods.  It  is  seldom  that  the  pul- 
monary second  sound  is  less  distinct  than  in  the  average  run  of  healthy  persons. 


152  Diseases  of  the  Heart. 

is  seen  in  solid  hypertrophy  of  the  left  ventricle.  In  con- 
sequence of  the  obstruction  in  front  (either  at  the  aortic 
orifice  itself  or  in  the  arterial  system  beyond)  the  contraction 
of  the  left  ventricle  is  more  deliberate  than  in  health,  and  the 
tension  of  the  mitral  segments  is  more  gradually  effected. 

Some  authorities  have  supposed  that  in  cases  of  this 
description,  the  left  ventricle,  in  consequence  of  being  over 
distended,  has  a  greater  difficulty  in  obtaining  a  'grip'  of  the 
blood,  so  to  speak,  than  it  has  in  health  ;  ^  and  that  this  is  the 
explanation  of  its  slow  and  gradual  contraction.  I  am,  how- 
ever, disposed  to  doubt  the  correctness  of  this  explanation. 
'  Loss  of  grip  '  would  be  much  more  likely  to  occur  in  dilata- 
tion than  in  solid  hypertrophy ;  and  dilatation  of  the  left 
ventricle,  as  we  have  already  seen,  tends  rather  to  produce 
accentuation,  at  the  same  time  that  it  shortens  the  duration 
of  the  first  sound. 

Others  have  explained  the  diminished  intensity  of  the 
mitral  first  sound  which  is  associated  with  some  cases  of 
hypertrophy,  by  supposing  that  the  'initial  tension'  of  the 
mitral  valve  is  so  great  that  the  contraction  of  the  ventricles 
docs  not  produce  the  usual  amount  of  tension,  and  therefore 
of  vibration  of  the  valve-segments.  In  other  words,  in  con- 
sequence of  the  excessive  intra-ventricular  pressure  during 
diastole, — a  condition  which  we  may  suppose  is  produced  by 
the  regurgitant  current  in  the  case  of  aortic  incompetence 
— the  segments  of  the  mitral  valve  are  closed,  and  partly 
stretched,  at  the  end  of  diastole,  i.e.  before  the  ventricular 
systole  occurs.- 

'  Solid  hypertrophy  always  results  from  some  obstruction  in  front.  The 
hypertrophy  which  occurs  in  mitral  and  aortic  regurgitation  is  always  associated 
with  some  dilatation. 

^  Increased  'initial  tension'  could  only  occur  in  aortic  regurgitation,  or  in  mitral 
lesions  in  which  the  blood  pressure  in  the  left  auricle  during  diastole  was  increased. 
Now,  in  mitral  regurgitation  the  first  sound  is  replaced  by  a  murmur  ;  and  in  mitral 
stenosis,  the  diminution  of  the  first  sound — which  is  certainly  present — is,  I  believe, 
due  partly  to  the  fact  that  the  mitral  segments  have  lost  their  normal  elasticity, 
partly  to  the  small  amount  of  blood  which  the  left  ventricle  contains,  and  there- 
fore to  the  diminished  force  with  which  the  mitral  segments  are  closed  and 
^•trctched. 


Altei'ations  in  the  duration  of  the  Heart  Sounds. 


:)5 


Another  reason,  which  has  been  advanced  as  a  partial 
cause  for  the  diminished  intensity  of  the  first  sound  in  cases 
of  soHd  hypertrophy  is,  that  the  sound  which  is  produced  by 
the  tension  of  the  mitral  and  tricuspid  valves  is  less  easily 
conducted  through  the  thick  muscle  of  the  ventricular  wall/ 
The  correctness  of  this  explanation  is,  in  my  opinion,  doubtful. 

Structural  alterations  which  impair  the  elasticity  of  the 
valve  segments  are  also  the  cause  of  diminished  intensity  of 
the  mitral  first  sound.  This  is  probably  one  of  the  conditions 
which  produce  the  modified  first  sound  which  occurs  in 
mitral  stenosis,  to  which  I  have  already  alluded. 

DiminisJied  intensity  of  tJie  tricuspid  first  sound. — Impair- 
ment of  the  force  of  the  right  ventricle  (fatty  degeneration, 
fibroid  degeneration),  and  dilatation  of  the  ventricular  cavity, 
are  the  chief  causes  of  this  condition.- 

Alterations  in  the  duration  of  the  Jieart  sounds. 

Alterations  in  duration  are  only  noticeable  in  connection 
with  the  first  sound.  It  may  be  either  longer  or  shorter  than 
in  health. 

Inereased  duration  of  the  first  sound  \?,  generally  associated 
with  the  slow  and  deliberate  contraction  which  is  seen  in 
solid  hypertrophy,  more  especially  with  the  solid  hyper- 
trophy which  is  caused  by  stenosis  of  the  aortic  orifice.  In 
addition  to  the  alteration  in  duration  the  sound  is,  in  these 
cases  (as  we  have  previously  seen)  more  mufiled  than  in  health. 

Diminished  duration  of  the  first  sound  is  generally  due  to 
dilatation,  or  dilatation  and  hypertrophy  of  the  left  ventricle, 
in  fact,  it  occurs  in  all  conditions  in  which  the  ventricular 
wall  is  enfeebled.  There  is  often  too,  in  such  cases,  an 
irritable  condition  of  the  cardiac  muscle,  which  produces 
increased  celerity  of  contraction.  These  alterations  are 
frequently  met  with  in  chlorosis  and  fatty  heart.^ 

'  Diagnosis  of  Diseases  of  the  Heart,  by  Dr  Sansom,  page  104. 

'  In  these  cases  tricuspid  regurgitation  often  occurs,  and  instead  of  a  weak 
first  sound  in  the  tricuspid  area,  we  have  a  tricuspid  systolic  murmur. 

'  In  the  more  advanced  stages  of  chlorosis  the  mitral  first  sound  may  be 
replaced  by  a  systolic  murmur. 


154  Diseases  of  the  Heart. 

Alterations  in  the  tone  of  the  heart  sounds. 

Alterations  in  tone  are  often  combined,  as  we  have 
already  seen,  with  alterations  in  intensity.  The  chief  modi- 
fications in  tone  are  as  follows  : — 

I.   The  heart  sonnets  may  be  more  mnffled  than  in  health} 

Muffling  of  the  first  sound  may  be  due  to  : — (a)  impaired 
conduction,  the  clinical  causes  of  which  have  been  already 
detailed  (see  page  149)  ;  (b)  weakness  of  the  walls  of  the  left 
ventricle  from  fatty  or  fibroid  degeneration,  etc.  ;  (c)  solid 
hypertrophy  of  the  left  ventricle  ;  and  (d)  alterations  in  the 
segments  of  the  mitral  valve,  which  impair  its  elasticity,  but 
which  do  not  give  rise  to  regurgitation. 

Muffling  of  the  aortic  second  sound  generally  results  from 
loss  of  elasticity  in  the  aortic  segments,  and  is  often  asso- 
ciated with  atheroma  of  the  base  of  the  aorta  and  disease  of 
the  coronary  arteries. 

Impnre  heart  sounds. — The  term  impurity  is  given  to  a 
modification  of  the  heart  sounds,  which  is  closely  allied  to 
muffling  on  the  one  hand  and  murmur  on  the  other.  In  fact 
an  impure  sound  may  be  described  as  a  sound  which  has  lost 
its  normal  well-defined  character,  which  is  usually  of  dimin- 
ished intensity,  and  which  is  somewhat  muffled  and  murmur- 
like. An  impure  sound  may  often  be  transformed  into  a 
murmur  by  exciting  the  heart  to  more  vigorous  action  — 
making  the  patient  walk  quickly  up  and  down  the  room, 
ascend  a  stair,  etc.- 

An  impure  sound,  then,  is  suggestive  of  valvular  imper- 
fection ;  and  the  presence  of  an  impure  aortic  second  sound, 
more  especially,^  may  be  a  physical  fact  of  great  practical 

'  Alterations  of  this  description  are  chiefly  important  in  connection  with  the 
mitral  and  aortic  sounds. 

-  I  must  caution  the  observer  against  over-exciting  the  heart  in  those  cases  in 
which  he  desires  to  produce  or  intensify  a  cardiac  murmur,  and  particularly  against 
applying  any  sudden  strain,  or  producing  any  sudden  rise  of  arterial  blood-pressure. 
An  American  traction  machine,  which  I  lately  saw  in  the  consulting  room  of  a 
well-known  London  physician,  seems  to  me  especially  dangerous,  and  verj'  likely 
to  produce  rupture  of  a  thin-walled  aneurism,  were  such  a  lesion  present. 

'  An  impure  first  sound  is  of  much  less  importance,  for  slight  incompetence  at 
the  mitral  or  tricuspid  orifices  is  frequently  due  to  temporary  and  curable  conditions. 


Alterations  in  the  tone  of  the  Heart  Sounds.      155 

importance.  (Impurity  of  the  aortic  second  sound  generally 
depends,  as  we  have  previously  seen,  upon  rigidity  of  the 
aortic  cusps  ;  and  rigidity  of  the  aortic  cusps  is  often  associ- 
ated with  atheroma  of  the  base  of  the  aorta  and  disease  of 
the  coronary  arteries,—  conditions  which  are  frequently  sus- 
pected, but  which  it  may  be  impossible  to  detect  by  means 
of  physical  examination.  Now,  in  more  than  one  case  of 
angina-like  pain  in  the  chest  which  has  come  under  my  own 
personal  observation,  the  presence  of  an  impure  aortic  second 
sound  was  the  only  physical  alteration  which  could  be 
detected,  and  as  we  shall  afterwards  see,  when  I  come  to 
treat  of  angina  pectoris,  the  recognition  of  disease  at  the  root 
of  the  aorta  is,  in  suspected  cases  of  that  disease,  a  point  of 
great  practical  importance.) 

2.  TJie  heart  sounds  may  be  more  aeeentuated  than  in 
Jiealth. 

The  conditions,  which  produce  modifications  of  this 
description,  have  already  been  considered,  and  need  not  again 
be  detailed  (see  p.  143). 

3.  Higli-pitcJied,  metallic,  auto-audible  heart  sounds. 
When    the    conditions    for    conduction    are     extremely 

favourable  ;  when,  for  instance,  that  portion  of  lung,  which 
covers  the  heart  and  great  vessels,  is  consolidated  or 
retracted,  the  heart  sounds  may  be  unusually  loud  and 
high-pitched.  A  loud  and  high-pitched  pulmonary  second 
sound,  for  example,  is  met  with  in  some  cases  of  pneumonia 
and  pleuro-pneumonia,  and  probably  depends,  as  Quincke 
was  the  first  to  point  out,  upon  retraction  or  consolidation  of 
the  portion  of  lung  which  overlaps  the  root  of  the  pulmonary 
artery. 

When  a  cavity,  well  suited  for  the  reproduction  and  con- 
duction of  sound,  is  in  contact  with  the  heart  or  great  vessels 
on  the  one  hand,  and  with  the  chest  wall  on  the  other,  the 
heart  sounds  may  have  a  metallic  or  amphoric  character.  In 
some  of  these  cases,^  and  in  some  cases  of  consolidation  of  the 

^  A  striking  example  of  auto-audible  heart  sounds,  depending  upon  the 
presence  of  a  cavity  in  the  lung,  is  described  by  Dr  Smith  in  the  Lancet  for 
December  i8,  i8So. 


156  Diseases  of  the  Heart. 

lung,  the  heart  sounds  may  be  auto-audible,  i.e.  heard  by  the 
patient  himself,  and  by  the  physician  without  applying  the 
ear  to  the  chest. 

A  striking  example  of  auto-audible  heart  sounds  depending  upon  con- 
solidation of  the  lung  came  under  my  observation  during  the  summer  of 
1 88 1.  A  patient  who  for  some  weeks  had  been  suffering  from  a  limited 
pleuro-pneumonia  of  the  left  base,  was  suddenly  seized  with  acute  pain 
m  the  left  side,  which  was  followed  by  quick  pulse,  elevation  of  tem- 
perature and  rapid  consolidation.  The  day  following  the  occurrence  of 
the  attack,  dulness  on  percussion  and  tubular  breathing  were  present 
over  the  lower  two-thirds  of  the  left  lung,  and  tJie  heart  sounds  could 
be  7-eadtly  Jieai'd,  ivlien  the  patient  sat  up,  ivitliout  applying  the  car  to  the 
chest. 

Rednp/icatioii  of  the  Heart  Sounds. 

We  have  previously  seen  that  although  four  sounds  (two 
first  and  two  second  sounds)  are  generated  within  the  heart, 
during  each  cardiac  revolution,  two  only  (a  single  first  and  a 
single  second  sound),  are,  under  ordinary  circumstances, 
heard  over  the  praecordia,  and  that  the  blending  of  the 
mitral  and  tricuspid  first  sounds  and  of  the  aortic  and 
pulmonary  second  sounds  is  due  to  the  fact,  that  the  action 
of  the  two  ventricles  is  usually  synchronous. 

Now,  under  certain  conditions,  even  in  health,  and 
not  unfrequently  in  disease,  two  first  sounds  or  two 
second  sounds  are  audible ;  and  the  heart  sounds  are 
said  to  be  reduplicated,  or,  as  Dr  Barr  prefers  to  term  it, 
duplicated. 

The  exact  cause  of  this  doubling  or  reduplication  has 
given  rise  to  great  debate,  but  most  authorities  are  agreed — 
and  with  their  opinion  I  entirely  concur — that  the  condi- 
tion is,  in  the  great  majority  of  cases,  due  to  a  synchronic 
closure  of  the  mitral  and  tricuspid  valve  flaps  ;  in  short,  that 
when  the  first  sound  is  reduplicated,  its  two  component  parts, 
viz.,  the  mitral  and  tricuspid  first  sounds,  are  individually 
audible  ;  and  that  when  the  second  sound  is  reduplicated, 
both  the  aortic  and  pulmonary  second  sounds  are  separately 
heard. 


Reduplication  of  the  First  Sound.  1 5  7 

It  will  be  advisable,  however,  to  consider  the  individual 
reduplications,  their  clinical  significance,  and  probable  causa- 
tion a  httle  more  in  detail.^ 


Reduplication  of  the  First  Sound. 

Reduplication  of  the  first  sound  is  rare — much  rarer  than 
reduplication  of  the  second  sound — a  circumstance  which  is 
probably  due,  as  Dr  Barr  has  suggested,  to  the  fact  that  the 
first  sound  is  produced  by  several  diff'erent  factors,  and  that 
it  is  a  sound  of  considerable  duration.  In  order  that  the  first 
sound  may  be  perceptibly  reduplicated,  i.e.  that  the  mitral 
and  tricuspid  first  sounds  may  be  separated  by  a  perceptible 
interval,  it  is  necessary  to  have  a  considerable  degree  of 
asynchronism  between  the  closure  and  tension  of  the  aortic 
and  pulmonary  valve  flaps — a  more  considerable  asynchron- 
ism than  is  required  to  produce  perceptible  doubling  of  the 
second  sound. 

Further,  I  am  of  opinion  that  reduplication  of  the  first 
sound  can  only  occur  when — in  addition  to  asynchronism — 
the  duration  of  one  or  other,  or  of  both  of  its  component 
parts  {i.e.  of  the  mitral  and  tricuspid  sounds)  is  lessened, 
or  when  the  duration  of  the  whole  cardiac  cycle  is  very 
considerably  increased  {i.e.  when  the  pulse  is  slower  than 
in  health).-     Under  ordinary   circumstances  the   first   sound 

'  While  I  am  of  opinion  that  asynchronism  is  the  cause  of  the  reduplication  in 
most  cases,  I  am  not  prepared  to  assert  dogmatically  that  it  is  so  in  all.  Some 
cases  are  with  difficulty  explained  by  this  view,  and  for  them,  some  of  the  many 
other  theories  which  have  been  advocated,  possibly  hold  true.  Space  does  not 
permit  me  to  consider  the  arguments  for  and  against  these  various  theories  in 
detail.  Those  readers  who  are  interested  in  the  subject  should  consult  the 
writings,  more  especially  of  Drs  Barr  and  Sansom,  where  they  will  find  full 
details. — (See  articles  in  the  Medical  Times  and  Gazette  of  January  and  February 
1877,  !^nd  in  the  Liverpool  Mcdico-Clm-tirgical  Journal,  July  1882,  by  Dr  Barr  ; 
and  Diagnosis  of  Diseases  of  the  Heart,  by  Dr  Sansom,  p.  106,  et  scq.) 

^  Asynchronism,  without  any  diminution  in  the  duration  of  the  mitral  and 
tricuspid  first  sounds,  might  account  for  the  condition,  if  the  duration  of  the 
whole  cardiac  revolution  [i.e.  of  the  diastolic  portion  of  the  revolution)  was  much 
increased  ;  if,  for  example,  the  heart  were  contracting  30  instead  of  72  times  in  a 
minute. 


1^8 


Diseases  of  the  Heai-f. 


occupies  (roughly)  ^■'yths  of  the  entire  cardiac  revolution.    (See 
fi&-  39-)      Now,  granting  that  the  tricuspid  first  sound—  as  is 


I'"in.   39. — Diagrammatic  representation  of  the  cardiac  cycle. 
I  =  first  sound. 
2=;second  sound. 
A=first  or  short  silence. 
B=second  or  long  silence. 

probably  the  case — is  of  somewhat  shorter  duration  than 
the  mitral  first  sound,  say  that  it  occupies  yVhs  of  the 
entire  cardiac  revolution,  it  is  almost  impossible  to  conceive 
that  reduplication  could  be  produced  by  asynchronism  alone, 
that  is  to  say,  that  reduplication  could  occur  in  any  case  in 
which  the  mitral  and  tricuspid  first  sounds  and  the  whole 
cardiac  cycle  (the  cycle  for  both  the  right  and  the  left 
hearts)  preserved  their  normal  length.  For  if  such  were  the 
case,  f'yths  4-  xV^'''  ^•^-  To^^^  ^^  ^^  entire  cardiac  revolu- 
tion, would  be  occupied  by  the  reduplicated  first  sound, 
and  to  this  we  must  add  the  interval  which  is  required,  i.e. 
which  must  separate  the  two  component  elements  of  the 
reduplicated  sound,  in  order  that  each  element  may  be  per- 
ceived as  a  separate  and  distinct  sound  by  the  ear.  Further, 
I  may  add,  that  reduplication  of  the  first  sound  can  never 
occur  when  the  heart  is  acting  quickly. 

The  three  conditions,  then,  which  I  believe  to  be  necessar}', 
in  most  cases,  for  perceptible  reduplication  of  the  first  sound 
are — 

(i)  Considerable  asynchronism  in  the  contraction  of  the 
two  ventricles. 

(2)  Diminished  duration  of  one  or  other  or  both  of  the 
component  parts  of  the  reduplicated  sound. 

(3)  Slow  action  of  the  heart. 


Reduplication  of  the  First  Sound.  159 

Numerous  other  theories  have  been  suggested  in  order  to  explain 
reduplication  of  the  first  sound,  viz. : — ■ 

1.  That  it  is  due  to  non-synchronous  tension  of  the  individual  seg- 
ments of  the  auriculo-ventricular  valves,  owing  to  the  absence  of  perfect 
uniformity  of  the  contraction  of  the  papillary  muscles. — {Gutimauii.) 

2.  That  the  reduplication  is  due  to  splitting  up  of  the  first  sound  into 
its  component  parts  of  ventricular  impulse  and  valve  tension.— (//cry^f^;?.) 

3.  That  it  is  due  to  a  double  mitral  valve  click,  the  true  mechanism  of 
which  remains  to  be  discovered. — {Professor  UEspine}) 

4.  '  That  the  contraction  of  a  dilated,  and  especially  of  a  hypertrophied 
left  auricle,  becomes  sonorous,  and  that  the  first  division  of  the  double 
first  sound  is  the  result  of  the  auricular  systole.' — {Dr  Geo)'ge  Johnson.) 

5.  '  That  it  is  due  to  a  presystolic  being  closely  followed  by  a  normal 
first  sound,  the  presystolic  sound  being  produced  by  the  sudden  floating 
upwards  of  the  mitral  curtains  occasioned  by  the  auricular  systole.' — {Dr 
Sansfl/n.) 

Dr  Barr  has,  I  think,  conclusively  disposed  of  these  various  theories, 
with  perhaps  the  exception  of  the  last,  in  the  article  to  which  I  have 
already  referred. — {Liverpool  Medico-Chirurgical  yournal.,  July  1882.) 

Dr  Sansofn's  theory  is  the  only  other  one,  in  addition  to  that  adopted 
in  the  text,  which  seems  to  me  at  all  probable.  He  explains  its 
mechanism  as  follows  : — '  During  the  interval  immediately  succeeding 
the  relaxation  of  the  ventricle,  the  blood,  subject  to  the  tension  in  the  left 
auricle  and  pulmonary  veins,  has  been  pouring  into  the  ventricular  cavity; 
the  fluid  naturally  finds  its  way  in  the  direction  of  least  resistance,  that  is, 
its  course,  when  impelled  towards  the  apex,  is  round  the  walls  of  the  ^-en- 
tricle,  thus  coming  behindxh^  curtains  of  the  mitral  valve,  and  bellying  them 
out  (so  to  speak)  as  the  sails  of  a  ship  are  bulged  by  the  force  of  the 
wind.  At  the  moment  of  auricular  systole,  the  ventricle,  as  yet  only 
partially  full,  is  rapidly  distended,  the  force  of  contraction  of  the  auricle 
giving  an  impulse  to  the  apex  of  the  ventricle,  and,  as  may  of  course  be 
inferred,  giving  a  contre-cotip  to  the  already  partially  strained  mitral 
curtains.  In  normal  conditions  such  contre-coup  is  inaudible,  but  when 
the  auricle  is  more  than  ordinarily  powerful,  or  when  the  mitral  valve  is 
so  changed  as  to  give  rise  to  the  sound  of  membranous  tension,  it  becomes 
perceptible  closely  preceding  the  sound  produced  by  the  ventricular 
systole — that  is,  the  sound  of  complete  closure  of  the  valves  guarding 
both  auriculo-ventricular  orifices  plus  the  muscular  sounds  of  the  ven- 
tricles.'— {Diagnosis  of  Diseases  of  the  Heart,  p.  115.) 

Doubling  of  the  first  sound  is  said  to  occur  physio- 
logically at  the  end  of  expiration  or  the  commencement  of 
inspiration  ;  and  pathologically  (though  rare)  it  has  been  met 
with  in  various  conditions,  amongst  which  the  following  are 


i6o  Diseases  of  the  Heart. 

the  chief: — functional  disorders  of  the  heart  ;  diseased  (de- 
generated) conditions  of  the  cardiac  muscle  ;  hypertrophy  of 
the  ventricles  ;  dilatation  of  the  ventricles  ;  valvular  lesions, 
more  especially  mitral  and  tricuspid  lesions. 

As  I  have  already  stated,  asynchronic  closure  of  the 
mitral  and  tricuspid  valves  is,  in  my  opinion,  the  most  im- 
portant cause  of  the  condition ;  and  we  must  now  consider 
how  the  asynchronism  may  be  brought  about. 

The  first  sound  oi  the  heart  is  probably  composed,  as  we 
have  previously  seen,  of  the  sounds  which  are  generated  by  : — 
{(i)  the  sudden  closure  and  tension  of  the  mitral  and  tricuspid 
valve  flaps  ;  {U)  the  contraction  of  the  ventricles  ;  and  (r)  the 
impulse  of  the  apex  beat  against  the  wall  of  the  chest ;  ^  and 
all  of  these  conditions  immediately  result  from  the  contrac- 
tion of  the  muscular  walls  of  the  ventricles,  which  is,  in  its 
turn,  due  to  the  rhythmical  discharge  of  motor  nerve  force 
in  the  cardiac  ganglia.  Further,  we  have  seen  that  the  ganglia 
are  stimulated,  to  discharge,  by  the  presence  of  blood  under 
a  certain  tension  in  the  cardiac  cavities,  and  that  the  action 
of  the  ganglia  can  be  held  back  (inhibited)  or  accelerated  by 
impulses  passing  to  the  heart  through  the  pneumogastric 
and  sympathetic  nerve  trunks. 

Now,  the  theory  which  explains  the  reduplications  of 
the  heart  sounds  by  asynchronic  closure  of  the  valve  flaps 
necessarily  presupposes  that  the  action  of  the  right  and  left 
ventricles  is  to  some  extent  at  least  independent,  and  that 
the  one  ventricle  may  begin  or  may  end  contraction  before 
the  other.'^ 


'  The  sudden  tension  of  the  valve  flaps  and  chordce  tendineae  is  probably  by 
far  the  most  important  factor  of  the  three. 

^  In  reference  to  this  part  of  the  subject  Dr  Barr  says:  '  In  reply  to  the  objec- 
tion which  has  been  urged  against  the  possibility  of  asynchronism,  on  account  of 
the  interlacement  of  the  cardiac  fibres  and  the  observed  consentaneousness  of  the 
ventricular  action,  I  say  that  I  have  seen,  felt,  and  heard  asynchronous  action, 
and  so  have  no  difficulty  in  admitting  the  possibility  of  its  occurrence.  I  do  not 
say  that  such  asynchronism  as  exists  between  the  auricles  and  ventricles  is  pos- 
sible between  the  two  ventricles,  but  I  do  say  that  each  side  of  the  heart  has  its 
own  proper  muscular  fibres,  as  well  as  those  which  are  common  to  both  sides ; 
and  those  proper  fibres  form  in  great  part  the  deepest  layers,  and  so  are  first 


Reduplication  of  the  First  Sound.  1 6  r 

Theoretically,  therefore,  we  may  suppose  that  redupli- 
cation of  the  first  sound  may  be  due  either  to  : — (A)  such 
accelerated  or  retarded  action  of  the  left  ventricle  as  is 
sufficient  to  cause  the  first  sound,  which  is  generated  within 
the  left  heart,  to  be  separated  by  an  interval,  sufficient  to  be 
appreciated  by  the  ear,  from  the  first  sound,  which  is  gener- 
ated within  the  right  heart  ;  or  to  (B)  such  accelerated  or 
retarded  action  of  the  right  ventricle  that  the  same  result — 
an  appreciable  interval  between  the  first  sounds  of  the  right 
and  left  hearts — may  occur.^ 

Further,  we  may  presume  that  accelerated  or  retarded 
action  of  either  ventricle  may  be  due  to  : — ■ 

I.  Differences  in  the  pressure  of  the  blood  in  the  two 
ventricles  by  reason  of  which  the  muscular  fibres  of  one  ven- 
tricle are  stimulated  to  contract  before  the  muscular  fibres 
of  the  other. 

It  is,  I  think,  highly  improbable  that  this  condition  alone 
is  ever  the  cause  of  a  reduplicated  first  sound — for,  as  we 
shall  see  when  I  come  to  speak  of  reduplication  of  the 
second  sound,  increased  pressure  of  the  blood  in  either  ven- 
tricle, generally  depends  upon  obstruction  in  front  ;  and  in 
such  conditions,  although  the  increased  blood  pressure  may 
stimulate  the  affected  ventricle  {i.e.  the  ventricle  which  has 
to  cope  with  the  difficulty,  and  in  which  the  increased  pres- 
sure occurs)  to  commence  contraction,  yet  by  reason  of  the 
obstruction  which  it  has  to  overcome,  it  is  longer  in  emptying 
itself,  and  in  such  cases  reduplication  of  the  first  sound  does 
not  of  course  occur. 


subjected  to  the  stimulating  influence  of  distention  in  producing  contraction ;  and 
in  those  fibres  which  are  common  to  both  sides,  it  is  possible  for  the  wave  of  con- 
traction to  commence,  as  it  were,  at  one  extremity  of  the  fibre  and  be  propa- 
gated to  the  other.  Each  side  has  more  or  less  independently  its  own  nerve 
supply,  its  own  peristaltic  action,  and  notwithstanding  that  both  sides  are  set  to  the 
same  time,  and  that  there  is  a  complex  interlacement  of  fibres,  yet  it  is  quite  pos- 
sible, nay,  it  is  an  experimental  fact,  that  one  side  may  begin  or  end  contraction 
before  the  other.' — {Liverpool  Medico-Chirurgkal  Joiiriial,  July  1882,  p.  206.) 

'  I  have  already  expressed  the  view  that  modifications  in  the  duration  of  the 
component  elements  of  the  reduplicated  sound,  or  of  the  duration  of  the  whole 
cardiac  cycle,  are  also  necessary. 

L 


1 62  Diseases  of  iJic  Heart. 

2.  Alterations  of  the  nerve  apparatus  of  one  ventricle,  by 
reason  of  which  the  motor  ganglia  of  one  side  are  rendered 
more  or  less  irritable  than  those  of  the  other.^ 

Such  a  condition  may  possibly  explain  the  reduplications 
of  the  first  sound,  which  are  said  occasionally  to  occur  in 
some  functional  (neurotic)  affections  of  the  heart. 

3.  Structural  alterations  of  the  muscular  fibres  of  one 
ventricle,  by  reason  of  which  its  contraction  is  more  or  less 
cjuickly  effected  than  that  of  the  other  ventricle.  In  some 
cases  of  fatty  degeneration  (in  the  early  stage  at  least)  a 
condition  of  '  irritable  weakness '  is  sometimes  met  with,  in 
which  the  muscular  fibre  is  more  easily  excited,  but  in  which 
its  contraction  is  less  sustained  {i.e.  of  shorter  duration)  than 
in  health.  It  is  easy  to  conceive,  therefore,  that  if  such  a 
change  were  confined  to  the  muscular  fibre  proper  to  one 
ventricle,  or  were  much  more  marked  in  one  ventricle  than 
in  the  other,  that  the  first  sound  produced  in  the  affected 
side  might  anticipate  that  produced  in  the  normal  one. 

So  again  in  cases  of  fibroid  degeneration,  the  contractility 
of  the  affected  ventricle  (granting  that  the  change  were 
confined  to  one  ventricle)  might,  we  can  easily  suppose,  be 
unduly  delayed,  and  therefore  sufficient  asynchronism  to 
cau.se  reduplication  of  the  first  sound,  produced. 

Reduplication  of  tJic  Second  Sound. 
Reduplication  of  the  second  is  much  more  frequent  than 
reduplication  of  the  first  sound.  It  occurs  as  a  physiological 
condition  at  the  end  of  inspiration  and  commencement  of 
expiration  ;  and  as  a  pathological  phenomenon  it  occurs  in 
many  different  conditions,  amongst  which  stenosis  of  the 
mitral  valve,  and  primary  obstruction  to  the  flow  of  blood 
through  the  lungs  (such  as  is  produced  by  cirrhosis,  emphy- 
sema, etc.)  are  the  chief.- 

'  If  Dr  Gaskell's  view — that  the  rhythmical  action  of  the  heart  is  due  to  a 
rhythmical  property  possessed  by  the  cardiac  muscle  itself,  independently  of  any 
ganglionic  nerve  apparatus — is  correct,  the  explanation  given  under  this  head  (2) 
will  not  of  course  hold  good. 

^  Reduplication  of  the  second  sound  occurs  in  at  least  one-third  of  all  the 
cases  of  mitral  stenosis,  and  is  highly  suggestive  of  that  condition. 


Reduplication  of  tJie  Second  Soiind.  i6 


o 


As  I  have  previously  stated,  I  agree  with  those  authori- 
ties who  beHeve  that  the  cause  of  reduplication  of  the  second 
sound  is  asynchronous  closure  (and  tension)  of  the  aortic 
and  pulmonary  valve  flaps  ;  and  we  may  theoretically  suppose 
that  the  asynchronic  closure  may  result  from  the  fact  that 
the  systole  of  either  ventricle  is  so  accelerated  or  so  delayed 
as  to  allow  of  an  appreciable  interval  between  the  recoil  of 
the  aorta  and  pulmonary  artery,  i.e.  between  the  production 
of  the  aortic  and  pulmonary  second  sounds. 

Further,  we  may  suppose  that  the  following  conditions 
may  produce  such  asynchronic  contraction  of  the  ventricles 
as  will  cause  reduplication  of  the  second  sound  : — 

1.  Derangement  of  the  nerve  apparatus  of  the  heart,  by 
reason  of  which  the  motor  ganglia  ^  of  one  ventricle  are 
rendered  more  irritable  or  less  irritable  than  those  of  the 
other.  This  is  probably  the  cause  of  the  reduplicated  second 
sound  which  is  not  uncommon  in  functional  (neurotic)  affec- 
tions of  the  heart. 

2.  Structural  alterations  of  the  muscular  fibres  proper  to 
either  ventricle,  by  reason  of  which  they  are  rendered  either 
more  irritable  or  less  irritable  than  in  health  ;  and  by  reason 
of  which  the  contraction  of  one  ventricle  is,  therefore,  unduly 
accelerated  or  unduly  retarded.     (See  remarks  on  page  i6i.) 

3.  Differences  in  the  pressure  of  the  blood  in  the  two 
ventricles,  by  reason  of  which  the  action  of  one  is  accelerated. 

Some  authorities,  who  allow  that  asynchronic  closure,  of 
the  aortic  and  pulmonary  valves,  is  the  cause  of  the  redupli- 
cation of  the  second  sound  in  mitral  stenosis,  have  supposed 
that,  in  consequence  of  tiie  increased  blood-pressure,  which  is 
present  in  the  right  chambers  of  the  heart,  the  right  ventricle 
is  first  stimulated,  that  it  first  completes  its  systole,  and  that 
the  first  element  in  the  reduplicated  sound  is  consequently 
pulmonic.  But  with  this  opinion  I  do  not  agree,  for,  as 
Dr  Barr  points  out,  it  does  not  necessarily  follow  th&t  the 

'  If  Dr  Gaskell's  view — that  the  rhythmical  action  of  the  heart  is  due  to  a 
rhythmical  property  possessed  by  the  cardiac  muscle  itself,  independently  of  any 
ganglionic  nerve  apparatus — is  correct,  the  explanation  given  under  this  head  will 
not  of  course  hold  good. 


164  Diseases  of  tJie  Heart. 

ventricle,  which  is  first  thrown  into  action,  will  first  com- 
plete its  systole  ;  for  the  duration  of  ventricular  systole  is  not 
a  fixed  quantity.  Further,  we  know  that  (within  the  range 
of  its  working  power)  the  duration  of  the  ventricular  systole 
varies  directly  with  the  amount  of  resistance,  which  has  to 
be  overcome  ;  in  other  words,  the  greater  the  resistance,  the 
longer  the  systole.  (Witness  the  slow  deliberate  pulse  of 
aortic  stenosis.)  And  many  good  clinical  observers  positively 
state  that  the  accentuated  element  of  the  reduplication  is  the 
second  element,  and  that  the  accentuated  or  second  element 
is  heard  over  the  area  of  the  pulmonary  artery  and  not  of  the 
aorta,  i.e.  that  it  is  pulmonary. 

4.  Differences  in  the  resistance  in  front,  by  reason  of 
which  the  systole  of  one  ventricle  is  rendered  of  shorter  or 
of  longer  duration  than  that  of  the  opposite  one. 

I  agree  with  Dr  Barr  and  others,  who  think  that  this  is 
the  true  explanation  of  the  reduplicated  second  sound  in 
mitral  stenosis — that  although  the  right  ventricle  is,  by  reason 
of  the  increased  blood-pressure  in  the  right  cavities  of  the 
heart,  first  stimulated  to  contract,  yet,  in  consequence  of  the 
obstruction  to  the  passage  of  the  blood  through  the  lungs, 
and  the  difficulty  which  the  ventricle  has  in  emptying  itself, 
its  systole  is  so  prolonged,  that  a  sufficient  amount  of  asyn- 
chronism  is  produced  to  allow  of  an  appreciable  interval 
between  the  aortic  and  pulmonary  sounds  ;  in  other  words, 
that  the  reduplication  is  primarily  due  to  alterations  in  the 
blood-pressure  of  the  aorta  and  pulmonary  artery  respect- 
ively, and  the  consequent  alteration  in  the  duration  of  the 
systole  of  the  right  and  left  hearts  ;  the  systole  of  the 
left  ventricle  being,  in  consequence  of  diminished  aortic 
pressure,  shorter,  while  the  systole  of  the  right  ventricle  is, 
by  reason  of  increased  pulmonary  pressure,  longer  than  in 
health. 

Numerous  other  tlieories  have  from  time  to  time  been  advocated 
to  explain  the  reduplication  of  the  second  sound,  amongst  which  the 
following  may  be  mentioned  : — 

I.  That  the  second  element  of  the  reduplication  is  produced  by  a 
sudden    tension    of  the   mitral    curtains    after  the  normal  second  sound 


Reduplication  of  the  Second  Sound. 


165 


has  occurred.  Dr  Sansom,  whose  theory  this  is,  gives  the  following 
explanation  of  it  : — '  It  seems  to  me,  therefore,  that  reduplication  of  the 
second  sound,  in  cases  of  mitral  stenosis,  can  be  best  explained  thus  : — 
The  first  element  of  the  reduplication  is  the  normal  second  sound ; 
the  tension  in  the  aorta  being  feeble,  it  is  the  pulmonic  element  which 
has  the  chief  share  in  the  production  of  such  second  sound.  The  second 
element  of  the  reduplication  is  the  sudden  tension  of  the  abnormal  mitral- 
curtains  produced  after  the  relaxation  of  the  left  ventricle.  I  am  not 
prepared  to  say  that  systole  of  the  auricle  is  esse7iiial  to  produce  this 
sudden  tension  ;  it  may  be  quite  possible  that  the  reaction  of  the  dis- 
tended pulmonary  veins  and  left  auricle  may  be  sufficient  to  cause  it. 
So  it  may  occur  previously  to  the  auricular  contraction,  the  latter 
occasioning  or  reinforcing  the  presystolic  murmur,  separated  by  a  slight 
interval  from  the  second  element  of  the  reduplication.' 

Dr  Sansom  illustrates  his  theory,  the  only  one  in  addition  to  that 
adopted  in  the  text  which  seems  to  me  probable,  by  the  following 
diagram  : — 


Fig.  40. — Diagram  illustrative  of  the  mechanism  of  pseudo-reduplication  of  the 
heart  sounds.     {After  Sansom). 

Ideal  section  through  the  left  auricle  (A)  and  left  ventricle  (V) ;  M.M,  mitral 
curtains  ;  the  arrows  show  the  direction  of  the  blood  current  during  the  ventricular 
diastole  and  auricular  systole. 


Diagnosis  0/  Diseases  of  the  Heart,  p.   1 20. 


1 66  r>isi-ascs  of  tJic  Heart. 

2.  Asynchronous  closure  of  the  indi\idual  segments  of  one  valve, 
aortic  or  puhnonary.  — (Guttmann.) 

3.  That  the  first  element  of  the  reduplication  is  the  *  audible  snap 
which  attends  the  systolic  closure  of  the  valve  segments,  separated,  by 
an  appreciable  interval,  from  the  diastolic  snap  (of  the  arterial  systole).' — 
(Dr  George  Balfour,  Lancet,  March  5,  188 1,  p.  396.) 

4.  That  the  reduplication  of  the  second  sound  originates  at  the 
narrowed  orifice  itself ;  and  that  the  two  elements  of  the  phenomenon 
in  question,  which  form  a  sound  which  is  always  more  or  less  muffled  and 
impure,  are  in  reality  the  component  parts  of  a  murmur. — (Guttmann — 
Hand-Book  of  Physical  Diagnosis,  p.  279.) 

5.  That  the  second  element  of  the  reduplicated  sound  is  the  sound 
which  is  produced  by  the  contraction  of  the  dilated  and  hypertrophicd 
left  auricle. — (Guttmann,  Handbook  of  Physical  Diagnosis,  p.  279.) 

ALTERATIONS    IN    THE    POSITION    OF   THE    HEART 
SOUNDS. 

The  heart  sounds  are  occasionally  heard  over  parts  of  the 
chest  at  which,  under  ordinary  circumstances,  they  are 
inaudible  or  only  faintly  heard.  As  a  rule,  such  sounds  are 
less  loud  than  the  sounds  heard  over  the  heart  itself;  but 
this  is  not  always  the  case,  and  it  occasionally  happens  that 
the  abnormally  placed  sound,  so  to  speak,  is  actually  louder 
than  the  heart  sounds  heard  over  the  prsecordia. 

The  conditions  which  give  rise  to  these  alterations  in  the 
position  of  the  heart  sounds  are  as  follows  : — 

1.  Anything  which  renders  the  tissues  and  parts  surround- 
ing the  heart  better  conductors  of  sound,  so  that  the  heart 
sounds  are  conveyed  to  parts  of  the  chest  at  which,  under 
normal  circumstances,  they  are  inaudible  or  only  faintly  heard'. 
Consolidations  of  the  lung,  tumours  in  the  mediastinum,  and 
curvatures  of  the  spine,  are  some  of  the  clinical  conditions 
which  are  included  under  this  head. 

2.  Changes  in  the  size  and  position  of  the  heart  itself. 
When,  for  instance,  the  left  ventricle  is  enlarged,  the  apex  is 
displaced  downwards  aiid  to  the  left,  and  the  heart  sounds 
are,  so  to  speak,  displaced  with  it.  So,  again,  when  the  heart 
is  pushed  to  the  right  by  an  extensive  left-sided  pleuritic 
effusion,  the  heart  sounds  may  be  inaudible  under  the  left, 
but  loudly  heard  under  the  right  nipple. 


Cardiac  ^hiruiurs.  167 

3.  Aneurisms  of  the  thoracic  aorta.  When  the  heart 
sounds  are  loudly  heard  over  a  part  of  the  chest  at  which, 
under  normal  circumstances,  they  are  faint  or  inaudible,  and 
when  the  abnormally  placed  sound  is  situated  over  the  course 
of  the  aorta,  the  presence  of  an  aneurism  should  be  suspected 
and  the  other  symptoms  and  signs  of  that  condition  carefully 
looked  for.  In  some  cases  of  this  description  the  heart 
sounds,  more  especially  the  second,  are  very  loud  {i.e.  accen- 
tuated), over  the  seat  of  the  tumour. 

ABSOLUTE   MODIFICATIONS   OF   THE   HEART    SOUNDS. 
MURMURS. 

The  alterations  of  the  heart  sounds  which  I  have  hitherto 
described  were  simple  or  quantitative  in  character ;  the  modi- 
fications which  we  must  now  consider  are  absolute  or  quali- 
tative. In  other  words,  the  normal  heart  sounds  are  either 
partly  or  entirely  replaced  by  new  sounds,  which,  in  normal 
conditions  {i.e.  in  conditions  of  perfect  health  and  during 
tranquil  action  of  the  heart)  are  never  heard  over  the  prs- 
cordia.  To  these  qualitative  modifications  the  term  niurviur 
is  given. 

Cardiac  uairinurs,  i.e.  new  sounds  heard  either  in  the 
place  of  or  along  with  the  heart  sounds,  may  be  produced 
either  outside  the  heart  or  in  the  heart  itself.  To  the  former 
the  term  cxo-cardial,  to  the  latter  etido-cardial,  is  applied. 

Exoca  rdial  Mu  rui  u  rs . 

Strictly  speaking  the  term  exo-cardial  murmur  should 
include  all  murmurs  produced  outside  the  heart,  but  as  a 
matter  of  fact  it  is  usually  limited  to  those  murmurs,  in 
reality,  friction  sounds,  which  are  synchronous  with  the  action 
of  the  heart,  and  which  are  produced  either  in  the  sac  of  the 
pericardium  or  in  the  adjacent  pleura,  i.e.  to  those  exo- 
cardial  murmurs  which  are  heard  over  the  praecordia.  Arterial 
and  venous  murmurs,  which  are,  of  course,  also  exo-cardial. 
are  classed  as  distinct.  It  is  in  the  usually  accepted — the 
narrow  and  restricted  sense — that  I  shall  make  use  of  the 
term. 


1 68  Vistasi's  of  tJie  Heart. 

Exocardial  murmurs,  then,  are  friction  sounds,  which 
are  synchronous  with  the  contractions  of  the  heart ;  usually 
double  (to-and-fro  sounds)  ;  generally  having  the  harsh,  grat- 
ing character  which  friction  sounds  commonly  possess  ;  as  a 
rule  heard  loudest  over  the  centre  of  the  heart,  i.e.  over  the 
anterior  surface  of  the  right  ventricle,  or  at  the  base  of  the 
organ  ;  almost  always  intensified,  and  sometimes  altered  in 
character  by  the  pressure  of  the  stethoscope  ;  and  which  are 
produced,  in  the  great  majority  of  cases,  by  the  rubbing 
together  of  the  inflamed  and  roughened  surfaces  of  the  peri- 
cardium. Exocardial  murmurs  are,  therefore,  almost  in- 
variably, indicative  of  pericarditis.^ 

Quite  exceptionally  a  friction  sound,  synchronous  with 
the  action  of  the  heart,  and  resembling  ver\-  closely  (it  may 
be  exactly)  the  to-and-fro  friction  murmur  of  pericarditis,  is 
produced  outside  the  sac  of  the  pericardium  by  the  rubbing 
of  the  roughened  outer  surface  of  the  pericardium  against  the 
front  wall  of  the  chest  or  adjacent  surface  of  the  pleura ;  and 
to  this  sound  the  term  pericardial-pleural-friction  iminmir  is 
applied.- 

Endocardial  Murmurs. 

Endocardial  murmurs,  i.e.  murmurs  which  are  produced 
within  the  heart  itself,  are  either  organic  ox  functional.  Under 
the  former  head  are  included  all  those  cases  in  which  the 
murmur  depends  upon  distinct  structural  alterations  (usually 
of  the  valvular  mechanism)  which  can  be  recognised  after 
death.  Under  the  latter  term,  i.e.  functional  murmurs,  it  is 
customary-  to  describe  those  cases  in  which  the  murmur 
depends  upon  temporary  and  curable  conditions,  or  in  which 
no   distinct   alteration    of    the    valvular    mechanism    can    be 


'  Exocardial  friction  murmurs  do  not  bear  such  an  exact  relationship  to  the 
sounds  of  the  heart  as  endocardial  murmurs.  They  are,  however,  as  stated  in 
the  text,  synchronous  with  the  cardiac  contractions — a  point  which  at  once 
distinguishes  them  from  ordinary  pleural  friction  murmurs. 

-  The  manner  in  which  the  pericardial-pleural-friction  murmur  is  to  be  dis- 
tinguished from  the  ordinary  friction  murmur  of  pericarditis  will  afterwards  be 
described.     (See  p.  327.) 


Mode  of  proditciion  of  Endocardial  Miirnuirs       1 69 

detected  after  death.  The  distinction  is  one  of  great  prac- 
tical utihty,  but  it  is  not  strictly  accurate  from  a  pathological 
point  of  view.  We  have  previously  s&er\,Jirst/y,  that  mitral  and 
tricuspid  regurgitation — conditions  which  are  attended  by 
well  marked  murmurs — frequently  result  from  'relative'  or 
'  muscular '  incompetence,  the  valve  segments  being  perfectly 
healthy  ;  and  secondly,  that  the  defective  muscular  action 
which  produces  the  incompetence,  depends  in  some  cases 
upon  temporary  and  curable,  in  others  upon  permanent  and 
incurable,  conditions.  Now,  in  both  cases,  the  murmur  is  un- 
doubtedly due  to  structural  alterations,  which,  provided  that 
the  patient  were  to  die  while  the  murmur  were  still  audible, 
could  be  recognised  on  the  post-mortem  table.  In  both 
cases,  therefore,  the  murmur  is,  strictly  speaking,  organic. 
Provided  that  this  fact  is  kept  in  view,  it  is  a  matter  of  prac- 
tical convenience  and  utility  to  describe  the  curable  cases  as 
functional,  and  the  incurable  as  organic. 

Before  we  consider  each  of  these  conditions  (organic  and 
functional  murmurs)  in  detail,  it  may  perhaps  be  well  to 
describe  the  manner  in  which  murmurs  are  produced. 

Mode  of  production  of  Endocardial  Murmurs. 

Endocardial   murmurs  are   due  to  the  production,  within 
the  heart,  of  vibrations  which  can   be   perceived  by  the  ear 
of  the  observer  ;    and   most    authorities  are  agreed  that  the 
audible  vibrations,  which  are  represented  externally  as  mur- 
murs, are  generally  (some  say  are  always)  due  to  the  produc- 
tion of  sonorous  fluid-veins  in   the  blood   itself     According 
to  M.  Chauveau,  these  sonorous  fluid-veins  are  always  gen- 
erated when    the   blood    stream    passes,   zuitk  sufficient  force 
from  a  part  of  the  circulatory  system  which  is  actually  or 
relatively  constricted,  into  a  part  which  (in  comparison  with 
the  part  behind  it)  is  actually  or  relatively  dilated  ;    as,  for 
,    instance,  when  the  blood  current  is  forcibly  driven  through  a 
,    constricted  mitral  orifice  into  the  ventricular  cavity  beyond. 
'  Other  authorities  suppose  that  the  blood  current  in  its  pas- 

I   sage  through  the  heart  may  throw  the  tissue  itself,  over  which 
j   it    passes,  into  vibration  ;   and  this  would  appear  to  be   the 


I  70  Diseases  of  iJic  Heart. 

manner  in  which  Dr  Austin    Flint  supposes   that   the  presys- 
toHc  murmur  of  mitral  stenosis  is  generated. 

The  vibration  of  a  filament  or  tongue  of  lymph  in  the 
blood  current  is  also  supposed  to  be  the  cause  of  some  auto- 
audible  and  musical  murmurs. 

Audible  vibrations  or  murmurs  may  probably  also  be 
produced  by  the  collision  of  two  opposing  blood  currents  ; 
when,  for  instance,  the  blood  stream  which  is  flowing  back- 
wards through  an  incompetent  mitral  orifice  meets  the  blood 
stream  which  is  advancing  into  the  left  auricle  from  the 
pulmonary  veins. 

The  fact  that  a  certain  intensity  of  blood  current  is 
necessary  for  the  production  of  a  murmur  is  a  point  of 
great  practical  importance.  We  frequently  find,  for  ex- 
ample, that  a  murmur,  which  depends  upon  organic  and 
permanent  conditions  {e.g.  the  presystolic  murmur  of  mitral 
stenosis)  disappears  as  the  case  progresses,  the  dilated  and 
weakened  auricle  (in  the  case  of  mitral  stenosis)  being  no 
longer  able  to  produce  a  blood  wave  capable  of  generating 
sound.  In  cases  of  this  description,  and  indeed  in  others,  in 
which  the  conditions  for  the  production  of  a  murmur  are  not 
as  yet  very  perfectly  developed,  we  can,  by  increasing  the 
force  of  the  heart's  action,  either  temporarily  by  exertion 
(walking  about,  ascending  a  stair,  etc.),  or  by  the  use  ot 
cardiac  tonics  (digitalis  for  example),  frequently  convert  an 
impure  or  ill-defined  sound  into  a  murmur,  and  can  thus  obtain 
important  diagnostic  evidence  as  to  the  nature  of  the  case. 

It  is  important,  too,  to  remember  that  the  composition  and 
quality  of  the  blood  seem  to  exercise  some  influence  in  the 
production  of  murmurs.  In  conditions  of  anaemia,  for  ex- 
ample, venous  murmurs  are  almost  invariably  present,  and  are 
without  doubt  due  to  the  abnormal  condition  of  the  blood.^ 

'  Dr  George  Balfour,  in  speaking  of  the  mode  of  production  of  the  venous  hum 
says,  '  As  a  venous  murmur  is  often  to  be  heard  in  certain  positions,  such  as  the 
torcular  Herophili,  where  no  other  change  is  at  all  probable,  under  all  the  circum- 
stances of  the  case,  except  one  involving  an  altered  relation  of  the  blood  to  its 
containing  vein,  we  can  have  no  hesitation  in  ascribing  its  production  to  that 
cause.  And  further,  from  what  we  know  of  the  mode  in  which  fluid  veins  are 
formed,  we  can  have  no  difliculty  in  saying  that  this  altered  relation  of  the  blood 


Organic  Endocardial  MiLrnmrs.  171 

It  is  possible,  too,  that  the  systolic  murmurs  which  are  so 
commonly  heard  over  the  base  of  the  heart,^  in  conditions  of 
anaemia,  are  in  part  at  least  due  to  the  same  cause.  But  to 
this  point  I  will  presently  recur. 

Organic  Endocardial  iMnrmurs. 

Organic  endo-cardial  murmurs  usually  depend  upon  some 
defect  in  the  valvular  mechanism  of  the  heart ;  occasionally 
they  are  due  to  congenital  imperfections  and  malformations  ; 
very  exceptionally  to  the  presence  of  clots  or  vibrating  fila- 
ments of  lymph  in  the  cardiac  cavities.  Organic  endo-cardial 
murmurs  are  in  the  adult  usually  heard  over  the  mitral  or 
aortic  orifices,  since  organic  lesions  of  the  valves,  which  are 
their  most  frequent  cause,  are  usually  left-sided  ;  but  they 
may  be  produced  at  any  of  the  cardiac  orifices.  They  are 
either  direct  or  indirect,  that  is  to  say,  they  may  be  produced 
either  by  the  blood  current  as  it  passes  onwards  in  its  natural 
forward  (direct)  course,  or  by  a  blood-current  passing  back- 
to  the  walls  of  the  vein  must  consist  in  the  production  of  increased  friction  between 
the  two,  so  that  in  those  positions  where  there  is  normally  a  relative  constriction, 
insufficient,  however,  to  produce  sonorous  veins,  the  increase  of  friction  between 
the  wall  of  the  vein  and  the  layer  of  blood  next  it  practically  narrows  the  opening 
sufficiently  to  do  so,  by  retarding  the  exterior  portion  of  the  blood  current  and 
leaving  the  central  or  axial  portion  uninfluenced.  Physical  laws  leave  no  doubt 
as  to  this.  It  is  for  physiologists  to  explain  whether  it  depends  simply  upon  a 
watery  condition  of  the  blood  or  upon  some  other  cause,  and  their  explanation 
would  no  doubt  be  of  the  greatest  importance  for  practical  medicine.' — Diseases  of 
the  Heart,  Second  Edition,  p.  170. 

'  As  we  shall  presently  see,  Dr  Balfour  is  of  opinion  that  the  basic  murmurs 
heard  in  the  earlier  stages  of  anaemia  are  due  to  mitral  regurgitation.  But  he  also 
admits,  that  in  the  later  stages,  arterial  murmurs  may  be  developed,  and  he  hints  at 
least  that  the  altered  condition  of  the  blood  may  play  some  part  in  their  production. 
He  says,  for  instance — '  Shortly  after  the  appearance  of  the  primary  hsemic  murmur, 
a  tricuspid  murmur  and  jugular  undulation  are  found  to  be  developed.  This  is 
naturally  accompanied  by  a  pulmonary  and  also  by  an  aortic  systolic  murmur,  the 
active  cause  in  the  production  of  both  these  murmurs  being  the  large  blood  waves 
sent  on  by  the  dilated  and  hypertrophied  ventricles.' — Ed.  Medical  Joiir.,  Oct. 
1882,  p.  295.  'There  is  also  an  abnormal  friction  between  the  spansemic  blood 
and  the  walls  of  the  blood-vessels,  hence  a  rise  in  arterial  blood -tension,  hence 
also  the  formation  of  fluid  veins  at  certain  favoural)le  points  within  the  venous 
lumen,  and  at  these  points  we  hear  the  primary  chlorotic  murmur — the  venous 
hum.' — Loc.  cit.,  p.  293. 


172  Diseases  of  the  Heart. 

wards    through    an    incompetent    valvular    orifice,    i.e.    by    a 
regurgitant  or  indirect  current. 

Tlie  points  to  be  observed  in  the  Clinieal  Investigation  of 
Cardiae  Murmurs  are  as  follows : — 

1.  The  rhythm  of  the  murmur. 

2.  Its  point  of  differential  maximum  intensity. 

3.  The  direction  in  which  it  is  propagated. 

4.  Its  sound  characters  (loudness,  tone,  pitch,  duration,  etc.) 

THE  RHYTHM  OF  THE  MURMUR. 

By  the  rhythm  of  the  murmur  we  mean  its  exact 
relationship  to  the  sounds  and  silences  of  the  heart.  The 
murmur  should,  if  possible,  be  '  timed  '  by  the  apex-beat,  and 
failing  this,  by  the  carotid  pulse.  When  the  heart  is  acting 
quickly,  it  may  be  very  difficult  or  even  impossible  to  'time' 
the  murmur  correctly.  The  difficulty  of  determining  the 
exact  rhythm  is  also  increased  where  more  than  one  murmur 
is  present,  and  this  is  more  particularly  the  case  where  a 
presystolic  is  combined  with  a  systolic  mitral  murmur  ;  the 
difficulty  being  less  in  the  case  of  double  aortic  murmurs, 
for  in  such  cases  the  interval  between  the  systolic  and 
diastolic  portions  of  the  murmur  is  usually  quite  distinct. 

Endocardial  murmurs  may  occur  either  during  the  systole 
or  the  diastole  of  the  heart,  i.e.  of  the  ventricles  ;  and  it  will 
now  be  necessary  to  consider  each  of  these  different  murmurs, 
and  the  conditions  which  may  produce  them,  in  detail. 

Systolie  Mnrniuys. 

Systolic  murmurs  correspond  to  the  contraction  or  systole 
of  the  ventricles  ;  they  more  or  less  completely  replace  the 
first,  or  systolic  sound  of  the  heart,  and  may  extend  into  the 
short  silence.     (See  fig.  41.) 

They  may  be  produced  either  in  the  left  or  right  heart, 
and  may  be  either  functional  or  organic.  They  represent 
one  or  other  of  the  following  conditions  : — 

I.  Regurgitation  through  the  auriculo-ventrieular  orijiees. — 
(Mitral   and   tricuspid    regurgitation.)     Both   of  these  condi- 


Sys^o/ic  Miirnutrs. 


17: 


Fui.  41. — Diagrammatic  representation  of  a  systolic  murmur,  replacing  the 
whole  of  the  first  sound.  The  murmur  in  this  and  succeeding  figures  is  repre- 
sented by  continuous  vertical  lines,  the  normal  sound  by  interrupted  horizontal 
lines.      I  =svstolic  murmur. 


tions  are  common.  The  former  (mitral  regurgitation)  is 
often  primary  ;  the  latter  (tricuspid  regurgitation)  is  usually 
secondary,  and  due  to  disease  of  the  mitral  valve,  or  to 
(primary)  obstruction  to  the  passage  of  the  blood  through 
the  lungs,  such  as  occurs  in  cirrhosis,  emph)'sema,  etc. 

Now  we  have  seen  that  auriculo-ventricular  regurgitation 
may  result  from  : — 

{a)  Organic  changes  in  the  valve  segments,  such  as 
puckerings,  contractions,  adhesions,  ruptures,  ulcerations  ; 
these  organic  changes  being  rare  on  the  right  side,  i.e.  at 
the  tricuspid  orifice. 

{b)  Muscular  incompetence,  i.e.  imperfect  closure  of  the 
valve  in  consequence  of  defecti\-e  muscular  contraction,  the 
valve  segments  being  healthy. 

{c)  Relative  incompetence,  i.e.  dilatation  of  the  valvular 
orifice,  the  valve  segments  being  healthy. 

And  since  both  'muscular'  and  'relative'  incompetence 
(which  are  often  present  in  the  same  case)  may  depend  on 
temporary  and  curable  conditions,  it  follows  that  auriculo- 
ventricular  regurgitation  may  be  either  organic  or  func- 
tional. 

2.  The  formation  of  a  fluid  vein,  or  the  production  of 
sonorous  vibrations  in  the  tissues  at  the  arterial  orifices 
(aortic  or  pulmonary  orifices),  or  in  the  first  part  of  the 
arterial  systems  {i.e.  in  the  commencement  of  the  aorta  or 
pulmonary  arter}'). 


I  74  Diseases  of  the  Heart. 

The  pathological  conditions  associated  with  these  basic 
systolic  murmurs  are  : — 

{a)  Constriction  of  the  arterial  orifices  (aortic  and  pul- 
monary stenosis).  Aortic  constriction  is  common,  pulmonary 
constriction  extremely  rare.  The  former  is  usually  acquired, 
the  latter  almost  always  congenital.^ 

{b)  A  tongue  of  lymph  adhering  to  the  arterial  (aortic  or 
pulmonary)  valve  flaps.  This  is  not  a  common  cause  of 
basic  systolic  murmurs,  but  it  does  sometimes  occur.  The 
murmur  which  it  produces  may  be  musical  and  auto-audible. 
It  may  disappear  in  the  course  of  treatment. 

(r)  Anaemia.  Basic  systolic  murmurs  are  common  in 
anaemia.  They  are  sometimes  heard  in  the  pulmonary, 
sometimes  in  the  aortic  area.  Their  exact  significance  and 
mode  of  production,  more  especially  of  the  systolic  murmurs 
heard  in  the  pulmonary  area,  have  given  rise  to  much  debate ; 
but  to  this  question — which  is  still  far  from  settled — I  shall 
presently  recur.     (See  page  i88.) 

id)  Dilatation  of  the  ascending  portion  of  the  aortic  arch. 
In  cases  of  this  description  the  aortic  orifice  is  usually 
diseased  (constricted).  A  murmur  may,  however,  be  pro- 
duced as  the  blood  passes  from  a  naturally  sized  aortic  orifice 
into  a  dilated  aorta  provided  that  it,  is  propelled  with  sufficient 
force  to  generate  an  audible  fluid  vein. 

It  is  obvious,  therefore,  that  systolic  murmurs  produced 
at  the  aortic  and  pulmonary  orifices  may,  like  those  produced 
at  the  mitral  and  tricuspid  orifices,  be  either  functional  or 
organic. 

Diastolic  Aliirnnirs. 

Diastolic  murmurs  occur  during  the  ventricular  diastole. 
There  are  at  least  three  distinct  varieties,  viz.  : — 

I.  The  diastolic  murmurs,  which  occur  during  the  period 
of  the  second  sound,  and  which  more  or  less  completely 
replace  it.  These  murmurs  may,  and  often  do,  extend  into 
the  second  or  long  pause.     (See  figs.  42  and  43.) 

'  In  some  cases  of  ulcerative  endocarditis  the  pulmonary  valve  is  afifected, 
and  a  systolic  pulmonary  murmur,  representing  pulmonary  stenosis,  is  observed. 
Such  cases  are,  however,  extremely  rare. 


Diastolic  M7irm2irs, 


175 


Fig.   42. — Diagrammatic  representation  of  a  diastolic  murmur,  replacing  second 
sound.     2  =  murmur. 


Fk;.  43. — Diagrammatic  representation  of  a  diastolic  murmur,  replacing  second 
sound,  and  extending  into  long  pause.     2  =  murmur  ;  B=long  pause. 

Novv^,  since  the  second  sound  of  the  heart  is  due  to  the 
closure  and  tension  of  the  aortic  and  pulmonary  valve  flaps 
it  follows,  that  a  murmur  which  replaces  the  second  sound 
must  represent  regurgitation  through  the  aortic  or  pulmonary 
valvular  orifices.  And  since,  as  a  matter  of  practical  expe- 
rience, we  know  that  pulmonary  regurgitation  hardly  ever 
occurs,  a  diastolic  murmur,  which  replaces  the  second  sound 
at  the  base,  is,  for  practical  purposes,  pathognomonic^  of  aortic 
regurgitation.  Further,  we  know,  as  a  matter  of  practical 
experience,  that  this  murmur  is  almost  invariably  organic. 
Aortic  regurgitation  generally  results  from  organic  changes 
in  the  aortic  segments  (contractions,  puckerings,  adhesions, 
ruptures,  ulcerations),  though  it  is  occasionally  due  to  dilata- 
tion  of  the  base  of   the    aorta,   the    valve    segments    being 


'  In  one  or  two  cases  a  diastolic  murmur  has  been  produced  in  an  aneurism 
independently  of  any  regurgitation  through  the  aortic  valves.  Such  a  condition 
is,  however,  so  extremely  rare,  that  for  practical  purposes  the  statement  in  the 
text — that  a  diastolic  basic  murmur  indicates  aortic  regurgitation— may  be  safely 
relied  upon. 


176  Diseases  of  tJie  Heart. 

perfectly  healthy,  ic.  it   is   occasionally  due   to   a  condition 
of '  relative  incompetence  '  of  the  aortic  orifice.^ 

2.  The  murmurs  which  occur  during"  the  latter  part  of  the 
long  silence  or  pause,  i.e.  immediately  before  the  systole  of 
the  ventricles,  and  to  which  the  term  presystolic  is  usually 
given.     (Fig.  44.) 


Fig.  44. — Diagrammatic  representation  of  a  presystolic  murmur. 

The  presystolic  murmur  stops  abruptly  with  the  systole 
of  the  ventricle,  i.e.  with  the  occurrence  of  the  first  sound  of 
the  heart  —  a  fact  which  is  at  once  explained  when  it  is 
understood  that  the  murmur  is  produced  by  the  formation  of 
a  fluid  vein  as  the  blood  is  forcibly  driven  by  the  contraction 
of  the  auricle  through  a  stenosed  mitral  orifice.^ 

Almost  all  authorities  are  agreed  in  thinking  that  the 
presystolic  or  auriculo-systolic  murmur  (as  Professor  Gairdner, 
who  was  one  of  the  first  to  direct  attention  to  its  true  signifi- 
cance, prefers  to  term  it),  is  always  due  to  organic  changes, 
i.e.  to  stenosis  of  the  mitral  or  tricuspid  orifices.  And  since 
tricuspid  stenosis  is  \^ery  rare,  a  pres\'stolic  or  auriculo- 
systolic  murmur,  in  the  great  majority  of  cases,  indicates 
mitral  stenosis. 

The  stenosed  condition  is  usually  due  to  adhesion  of  the 
cusps,  the  chordae  tendineai  are  often   thickened,  and  some- 

'  This  condition  is  (?)  always  associated  with  organic  changes  at  the  root  of 
the  aorta  ;  but  it  is  quite  possible,  as  Dr  George  Balfour  points  out,  that  a  dilated 
aorta  may  contract,  and  so  the  condition  of  incompetence  be  removed.  '  Relative 
incompetence '  of  the  aorta  depends  then  upon  organic  changes,  but  it  may  some- 
times disappear  under  treatment. 

-  In  some  cases  of  presystolic  murmur,  i.e.  of  mitral  constriction,  the  first 
sound  of  the  heart  is  replaced  by  a  systolic  murmur,  and  the  presystolic  therefore 
passes  into  the  systolic  murmur  {i.e.  is  continuous  with  it),  the  two  murmurs  being 
as  a  rule  distinguishable  by  their  sound  characters. 


Presystolic  Muinnurs.  177 

times,  as  it  were,  fused  into  a  mass  with  the  cusps  and  papil- 
lary muscles.  The  stenosis  is  sometimes  due  to  calcareous 
deposits  in  the  base  of  the  valve  and  in  the  valve  segments  ; 
occasionally  a  mass  of  vegetations  obstructs  the  orifice  ;  in 
rare  cases  the  stenosis  is  caused  by  the  pressure  of  a  tumour, 
the  valve  segments  being  perfectly  healthy. 

.Professor    Austin    Flint    differs    from    the    generally    ac- 
cepted opinion,  viz.,  that  a  presystolic  murmur  is  invariably 
organic.       While    granting    of    course    that    the    murmur    is 
generally    due    to    mitral     stenosis,    he    thinks    it     by    no 
means  pathognomonic  of  that  condition.     He   believes  that 
it   may  occur  independently   of  any   mitral    lesion,   and    he 
has   recorded  several  cases   in   support   of  his   view.     In   all 
these  cases  there  were  aortic  lesions  permitting  of  regurgita- 
tion ;  and  the  question  at  once  suggests  itself,  whether  the 
presystolic  murmur  heard  at  the  apex  was  produced  at  the 
mitral    orifice    at    all.     Might   it    not   have    been    the  aortic 
murmur  heard  at  the  apex  of  the  heart .''     The  explanation 
which  Professor  Flint  gives  of  the  production  of  the  murmur 
in  such  cases  is  as  follows: — 'With  regard  to  this  specimen, 
consider  the  physical  conditions  in  life,  at  the  instant  when 
the  auricular  contraction  took  place.     The  left  ventricle  was 
filled  with  blood  from  the  current  passing  from  the  auricle 
to  the  ventricle,  through  an  unobstructed  orifice,  by  gravita- 
tion, and  in  addition  by  the  regurgitant  current  from  the  aorta. 
As  a  consequence  the  mitral  curtains  were  floated  away  from 
the  ventricular  walls,  and  were  not  only  approximated  but 
in  absolute  contact.     Recollect  the  physiological  experiment 
by   which   it  is   shown   that   the   mitral  valve   may   be   com- 
pletely   closed    by    injecting    liquid    into    the    left    ventricle 
through  the  mitral  orifice.      These  conditions  existing,  the 
auricle  contracts  and  forces  an  additional  quantity  of  blood 
into  the  ventricle.     This  mitral  direct  current  passes  between 
the   valvular  curtains   which   are  in   apposition,   and   throws 
them  into  vibration  precisely  as  the  lips  are  made  to  vibrate 
with  the  breath.'  ^ 

3.  The  murmurs  which  occur  during  the  first  part  of  the 

'  Lancet,  Jan.  27,  18S3. 
M 


178 


Diseases  of  the  Heart. 


long   pause,   but   which   follow,  usually  with   a   distinct   and 
appreciable  interval,  the  second  sound.     (See  fig.  45.) 


Fir,.  45. — Diagrammntic  representation  of  post-diastolic  murmur,  which  occurs 
in  some  rare  cases  of  mitral  stenosis.  It  is  separated  from  the  commencement  of 
the  first  sound  by  an  appreciable  interval. 

This,  which  is  by  far  the  rarest  form  of  diastolic  murmur, 
is  occasionally  met  with  in  mitral  stenosis,  and  is  doubtless 
produced  by  the  blood  which  has  been  pent  up  in  the  left 
auricle  and  parts  behind  it,  during  the  ventricular  systole, 
i.e.  while  the  mitral  valve  was  closed,  being  propelled  with 
sufficient  force  through  the  stenosed  orifice  to  produce  a  fluid 
vein,  i.e.  to  generate  a  murmur.  Possibly  too  the  negative 
pressure  in  the  ventricle,  i.e.  the  suction  which  occurs  when 
the  ventricle  relaxes,  aids  in  the  production  of  the  murmur.^ 

The  period  at  which  the  murmur  occurs,  i.e.  during  the 
first  part  of  the  long  pause,  clearly  shows  that  the  contrac- 
tion of  the  auricle,  which  does  not  occur  until  the  end  of  the 
long  pause,  takes  no  part  in  its  production. 


Combination  of  Murmurs.— \x\  many  cases  more  than  one 
murmur  is  present.  (See  figs.  46,  47,  48.)  An  aortic  systolic 
murmur  is  very  often  combined  with  an  aortic  diastolic 
murmur,  and  a  mitral  presystolic  murmur  with  a  mitral 
systolic.  Further,  in  advanced  cases  of  aortic  regurgitation, 
the  mitral  valve  often  becomes  incompetent,  and  a  systolic 
mitral  murmur  is  heard  in  addition  to  the  aortic  diastolic 
murmur  which   was   present  from   the  first.      Again,   in   the 

'  Goltz  and  Gaule  believe  that  the  negative  pressure  appears  at  the  beginning 
of  the  diastole,  and  that  it  is  caused  by  the  expansion  of  the  ventricle.  '  Were 
this  the  case,'  says  Prof.  Michael  Foster,  'the  ventricle  might  be  regarded  not 
only  as  a  force  pump  driving  blood  into  the  arteries,  but  also  as  a  suction  pump 
drawing  blood  from  the  auricles  and  great  veins.' — A  Text  Book  of  Physiology, 
Fourth  Edition,  p.   152. 


I 


Combinafion  of  Miirmitrs. 


^79 


advanced  stages  of  mitral  lesions,  tricuspid  regurgitation  fre- 
quently results  from  the  secondary  changes  which  are  estab- 
lished in  the  right  heart ;  while  in  cases  of  anaemia,  systolic 
murmurs  are  sometimes  heard  at  all  the  cardiac  orifices 


Fig.   46. — Diagrammatic  representation  of  systolic  and  diastolic  murmur. 


ft 


Fig.   47. — Diagrammatic  representation  of  systolic  and  presystolic  murmurs. 


Fig.   4S. — Diagrammatic  representation  of  systolic,  diastolic,  and  presystolic 

murmurs. 

It  is  sometimes  doubtful  whether  a  cardiac  sound  is 
replaced  or  only  obscured  by  a  murmur,  and  in  the  case  of 
all  murmurs  it  is  desirable,  if  possible,  to  determine  whether 
any  cardiac  sound  still  remains.  Now  these  points  can,  as 
Gendrin  was  the  first  to  point  out,  sometimes  be  ascertained 
by  removing  the  ear  a  short  distance  from  the  end  of  the 
stethoscope,  or  by  so  placing  the  instrument  that  the  ear- 
piece only  partly  covers  the  external  auditory  meatus.  By 
this  means  the  sound  is  rendered  more  audible,  while  the 
murmur  becomes  less  distinct. 

The  fact,  that   the  heart  sound  is  heard,  as  well  as  the 


i8o  D/scciscs  of  the  Heart. 

murmur,  shows,  more  especially  in  the  case  of  diastolic  aortic 
murmurs,  that  the  valvular  segments,  or  some  of  them,  can 
still  be  closed  and  put  upon  the  stretch,  in  fact,  that  they  are 
still  capable  of  generating  the  second  sound.  It  does  not 
however  follow  that  in  such  cases  the  lesion  is  a  trivial  one. 
In  fact,  in  some  cases  in  which  one  valve  segment  only  is 
affected  (as  in  a  case  which  I  shall  afterwards  relate),  the 
contrary  holds  good.  The  fact,  then,  that  some  sound  re- 
mains, suggests  that  some  of  the  valve  segments  are  still 
sufficiently  healthy  to  generate  the  normal  sound.  When 
the  disease  has  developed  slowly,  as  in  atheromatous  disease 
of  the  valve,  it  is  probably  a  favourable  indication,  and  shows 
that  the  valve  is  not,  as  yet,  very  seriously  affected.  In  acute 
cases — such  as  traumatic  rupture  of  a  valve  segment,  or 
ulceration  of  the  segments — it  may  be  of  no  value  whatever, 
but  this  point  will  be  more  fully  discussed  in  treating  of  the 
prognosis  of  aortic  regurgitation.^ 

THE  POINT  OF  DIFFERENTIAL  MAXIMUM    INTENSITY  OF  THE 

MURMUR. 

From  what  I  have  previously  stated  in  speaking  of  the 
differential  maximum  intensity  of  the  normal  heart  sound 
(see  page  138),  it  will  readily  be  understood  that  in  order  to 
ascertain  the  valvular  orifice  at  which  the  murmur  is  pro- 
duced, it  is  necessary  to  ascertain  its  point  of  differential 
maximum  intensity.  These  points  are  shown  in  the  diagrams 
(figs.  49  to  54),  and  are  as  follows  : — 

Mitral  Minima's. — The  point  of  differential  maximum 
intensity  of  mitral  murmurs  is  the  left  apex-beat,  wherever 
it  may  happen  to  be,  not  necessarily  in  the  fifth  left  inter- 
space, an  inch  and  a  half  below,  and  slightly  internal  to  the 
left  nipple,  i.e.  the  position  of  the  apex-beat  in  health.  (See 
fig.   49.)     Presystolic   mitral   murmurs   are  often   best   heard 

'  The  observer  must  of  course  satisfy  himself  that  the  sound  which  remains  is 
generated  at  the  affected  vahailar  orifice.  In  the  case  of  an  aortic  diastolic 
murmur,  for  instance,  a  second  sound,  due  to  closure  of  the  pulmonary  flaps, 
might  be  heard  in  some  situations  along  with  the  diastolic  murmur,  and  might  be 
referred  to  the  aortic  orifice. 


Points  of  viaxinuiui  intensity  of  MnrnitLrs.      i8i 

slightly  internal  to  or  just  above  the  position  of  the  apex-beat, 
rather  than  at  the  apex-beat  itself.     (See  fig.  50.) 

Aortic  Munnurs.  —  The  point  of  differential  maximum 
intensity  of  aortic  murmurs  is  the  second  right  costal  cartilage 
at  its  junction  with  the  sternum  (the  aortic  cartilage).  A 
diastolic  aortic  murmur  may  however  be  heard  loudest  at  the 
lower  end  of  the  sternum,  in  consequence  of  the  fact  that 
it  is  propagated  downwards  in  the  course  of  the  blood  current 
which  produces  it.     (See  figs.  51  and  52.) 

Pulmonary  Murjniirs. — The  point  of  differential  maximum 
intensity  of  pulmonary  murmurs  is  the  third  left  costal 
cartilage  at  its  junction  with  the  sternum  (the  pulmonary 
cartilage).     (See  fig.  53.) 

Tricuspid  Ahirmurs. — The  point  of  differential  maximum 
intensity  of  tricuspid  murmurs  is  the  lower  end  of  the 
sternum,  or  rather  the  junction  of  the  lower  left  cartilages 
with  the  sternum.  (See  fig.  54.)  Some  authorities  place  the 
point  of  differential  maximum  intensity  for  tricuspid  murmurs 
at  the  junction  of  the  lower  riglit  costal  cartilages  with  the 
sternum. 

A  systolic  murmur  is  sometimes  heard  equally  loud 
at  the  base  and  at  the  apex  of  the  heart,  and  it  may  be 
difficult  or  impossible  to  determine,  from  its  mere  loudness, 
at  the  two  points,  whether  it  is  generated  at  the  aortic  or  at 
the  mitral  orifice,  or  at  both,  i.e.  whether  there  are  two 
separate  murmurs.  The  question  must  be  decided  in  the 
following  manner : 

Firstly.  The  murmur  must  be  carefully  traced  from  one 
point  to  the  other — from  the  apex  to  the  aortic  cartilage,  for 
example,  in  the  case  we  are  supposing.  If  the  intensity  of 
the  murmur  diminishes  at  a  point  midway  between  the  two 
positions  {^i.e.  the  two  points  of  differential  maximum  inten- 
sity), there  are  probably  two  murmurs. 

Secondly.  The  tone  of  the  murmur  at  the  two  points  must 
be  carefully  noted.  If  the  tone  differs  there  are  probably  two 
murmurs. 

Thirdly.  The  direction  of  propagation  must  be  observed. 


1 82  Diseases  of  the  Heart. 

If  the  murmur  is  well  propagated,  both  upwards  over  the 
aorta,  and  outwards  and  upwards  towards  the  axilla,  there 
are  in  all  probability  two  murmurs. 

THE  DIRECTION  IN  WHICH  THE  MURMUR  IS  PROPAGATED. 

Murmurs  are  propagated  chiefly  in  two  ways,  viz. : — (i)  B}- 
conduction,  i.e.  through  the  structures  in  which  they  are  ge- 
nerated, and  by  the  parts  which  surround  those  structures. 
{2)  ^y  convection,  i.e.  carried  by  fluid  in  the  direction  in  which 
it  is  flowing.  As  a  matter  of  practical  experience  and  obser- 
vation, we  know  that  the  different  murmurs  which  represent 
different  vahailar  lesions,  are  propagated  in  certain  definite 
directions,  which  are  as  follows  : — 

Mitral  regU7-gitant  {systolic)  uiiirninrs  : — These  murmurs 
are  propagated  upwards  and  outwards  towards  the  left  axilla 
(see  fig.  49) ;  and,  when  organic,  are  often  well  heard  at  the 
inferior  angle  of  the   left  scapula.      According   to   Naunyn, 


Fig.  49.— Outline  figure  showing  point  of  diflerential  ma.ximum  intensity  (*) 
of  the  systolic  mitral  murmur  (mitral  regurgitation);  and  the  direction  in  which 
it  is  propagated.  The  cross  +  ,  which  is  supposed  to  represent  the  normal  position 
of  the  apex-beat,  is  placed  a  little  too  high. 


Direction  of  propagation  of  Murinurs.  18 


J 


Balfour,  and  others/  the  systolic  murmur,  due  to  mitral  rei^ur- 
g-itation,  is  sometimes  heard  in  the  region  of  the  pulmonar)- 
artery,  being  conducted  to  that  part  of  the  chest  through  a 
dilated  left  auricular  appendix. 

Mitral  direct  {presystolic^  ninruiur.  —  This  murmur  is 
usually  heard  over  a  very  limited  area.  The  blood  current, 
which  produces  it,  is  flowing  directly  towards  the  apex  (or 
very  nearly  so)  of  the  heart.  (See  fig.  50.)  We  can  readily 
understand  therefore  why  the  presystolic  murmur  is  usually 
limited  to  the  position  of  the  apex  beat. 


Fig.  50. — Outline  figure  showing  point  of  differential  maximum  intensity!*) 
of  the  presystolic  mitral  murmur  (mitral  stenosis) ;  and  the  direction  in  which  it  is 
propagated.  (The  murmur  is  often  best  heartl  a  little  above  and  internal  to  the 
apex-beat,  which  in  the  diagram  corresponds  to  the  star.*) 

Aortic  regurgitant  {diastolic)  murmurs  are  carried  down- 
wards by  the  blood  current  which  produces  them,  towards 
the  apex  of  the  heart  ;  but  in  consequence  of  the  fact  that 
the     sternum    is    such    a    good     conductor    of    sound,    these 

'  These  writers  say  that  the  murmur  is  not  heard  exactly  over  the  pulmonary 
area,  but  a  little  outside  it,  viz.,  at  a  spot  an  inch  and  a  half  outside  the  sternum, 
in  the  third  interspace,  just  at  that  spot  at  which  the  tip  of  the  left  auricular 
appendix  comes  forward  from  beneath  the  cover  of  the  pulmonary  artery. 


184  /h'seascs  of  ihc   Heart. 

nuirmurs  are  well  conducted  down  that  bone,  and  are  often 
heard  very  distinctly  at  the  xiphoid  cartilage,  as  represented 
in  fig.  51. 


Fn;.    51. — Outline  figure  showing  point  of  differential  maximum  intensity  (*) 
of  the  diastolic  murmur  (aortic  regurgitation);   and  the  direction  in  which  it  is 

propagated. 

Aortic  direct  {systolic)  murmurs  are  carried  upwards  over 
the  course  of  the  aorta,  and  the  great  branches  which  arise 
from  it.  Organic  murmurs  are  more  extensively  carried  in 
these  directions  than  functional,  i.e.  anaemic  murmurs.  (See 
fig-  52.) 

Pulmonary  regurgitant  {diastolic)  murmurs  are  so  ex- 
tremely rare,  that  for  practical  purposes  they  may  be  almost 
ignored,  they  are  propagated  downwards  towards  the  lower 
end  of  the  sternum. 

Pulmonary  direct  {systolic)  murmurs,  which,  when  organic, 
are  extremely  rare,  are  propagated  upwards  and  outwards, 
over  the  course  of  the  pulmonary  artery.  As  a  rule  they 
cannot  be  traced  for  any  distance  over  the  surface  of  the 
chest.     (See  fig.  53.) 


Direction  of  propaoation  of  Mitrnntrs.  i8- 


Fig.  52. — Outline  figure  showing  point  of  differential  maximum  intensity  (*) 
of  the  systolic  aortic  murmur  (aortic  stenosis)  ;  and  the  directions  in  which  it  is 
propagated. 


Fig.    53. — Outline  figure  showing  the  point  of  difierential  maximum  intensity  of 
the  systolic  pulmonary  murmur,  and  the  direction  in  which  it  is  propagated. 


i86  Diseases  of  the   Heart. 

Tricuspid  regurgitant  {systotic)  munniirs  are  not,  in  my 
experience,  extensively  propagated  over  the  chest,  but  are 
usually  heard  over  a  limited  area.  The  direction  of  their 
propagation  is  probably  that  shown  in  fig.  54. 


Pig.    54. — Outline  figure  showing  point  of  dift'erential  maximuiu  intensity  C*)  of 
the  systolic  tricuspid  murmur. 

Tricuspid  direct  (^presystolic^  viurvnirs  are  extreinely  rare, 
they  would  probably  be  propagated  towards  the  apex  of  the 
heart. 

THE  SOUND  CHARACTERS  OF  THE  MURMUR. 

Some  murmurs  are  soft  and  blowing  ;  others  are  harsh 
(grating,  rasping,  filing,  sawing,  etc.)  in  character ;  others 
again  are  whistling,  cooing,  and  musical.  Occasionally,  as 
I  have  before  mentioned,  a  murmur  is  auto-audible. 

Inorganic  murmurs  are  usually  soft  ;  'direct'  murmurs  {i.e. 
murmurs  due  to  obstruction  at  one  or  other  of  the  cardiac 
orifices)  are  usually  harsher  and  rougher  than  'indirect' 
ones  {i.e.  murmurs  due  to  regurgitation).  But  speaking 
generally,  it   may  be  said  that  the   mere  sound   character  of 


Functional  Mumnurs.  187 

the  murmur  is  not  a  point  of  much  practical  importance/ 
either  from  a  diagnostic  or  a  prognostic  point  of  view;  and  this 
is  readily  understood  when  it  is  remembered  that  the  sound 
characters  of  the  murmur,  more  especially  its  loudness,  are 
largely  due  to  the  force  of  the  blood  current  which  produces 
it ;  in  other  words,  the  loudness  of  the  murmur  depends  to 
a  great  extent  upon  the  condition  of  the  cardiac  muscle. 
When  the  muscular  wall  of  the  heart  is  weakened  or  degene- 
rated, the  murmurs  which  are  generated  are  faint  and  soft  ; 
and  in  advanced  cases,  as,  for  instance,  in  extreme  cases  of 
mitral  stenosis,  no  murmur  may  be  generated  at  all.  And 
since  a  weakened  and  degenerated  condition  of  the  heart 
muscle  may  be  due,  either  to  temporary  and  curable,  or  to 
permanent  and  incurable  conditions,  it  follows  that  the  soft- 
ness and  faintness  of  the  murmurs,  which  are  produced  by 
Its  contraction,  cannot  be  relied  upon  as  any  indication  of  the 
severity  of  the  lesion. 

When,  however,  a  harsh  nnirmur  gradually  becomes 
fainter  and  softer,  we  may,  as  a  general  rule,  conclude  that 
the  strength  of  the  muscular  wall  is  diminishing,  and  we 
may  be  pretty  sure  that  this  is  the  case,  when  the  symptoms 
are  at  the  same  time  increasing  in  severity.  A  faint  murmur, 
then,  associated  with  severe  symptoms,  is  usually  indicative 
of  a  grave  lesion. 

FUNCTIONAL    MURMURS. 

It  is  customary  to  include  under  the  term  functional 
murmurs,  all  those  cases  in  which  the  murmur  depends  upon 
temporary  and  curable  conditions,  or  in  which  no  distinct 
alteration  in  the  valvular  mechanism  (it  would  perhaps  be 
more  correct  to  say  in  the  valvular  segments)  can  be  detected 
after  death.  Functional  murmurs  are  always  systolic  in  time, 
and  are  generally  heard  at  the  base  of  the  heart,  most  com- 
monly to  the  left  of  the  sternum,  in  the  second  interspace,  i.e. 
in  the  region  of  the  pulmonary  artery.  They  are  sometimes 
also  heard  in  the  aortic,  mitral,  and  tricuspid  areas. 

'  The  presystolic  murmur  is  a  notable  exception.  In  typical  cases  the  sound 
characters  of  the  murmur  (as  I  shall  afterwards  describe  in  detail)  are  so  distinct 
as  to  distinguish  it  from  all  other  cardiac  murmurs. 


1 88  Diseases  of  the  Heart. 

The  exact  significance  and  mode  of  production  of  the 
functional  murmurs,  which  are  audible  at  the  base  of  the  heart, 
have  given  rise  to  great  debate,  and  are  among  the  most 
unsettled  points  in  cardiac  pathology. 

VValshc  divides  the  so-called  functional  murmurs  into  two 
great  groups,  which  he  respectively  terms  haemic  and  dynamic. 
Under  the  former  he  places  'murmurs  originating  within  the 
heart  and  dependent  upon  an  unnatural  state  of  the  blood  ; ' 
while  under  the  latter  he  includes  '  murmurs  which  result 
from  abnormal  action  on  the  part  of  the  heart,'  the  proper 
valvular  mechanism  being  healthy.  And  this  division  in- 
dicates the  two  great  causes  of  functional  murmurs,  viz.: — 
(i)  defective  muscular  action  d\\o\\\x\^  oi  mitral  and  tricuspid 
regurgitation  ;  and  (2)  an  altered  condition  of  the  blood, 
which  probably  aids,  at  least,  in  the  production  of  the  pul- 
monary and  aortic  murmurs,  which  are  met  with  in  con- 
ditions of  anaemia. 

But  it  will  be  necessary  to  consider  the  subject  in  more 
detail.  Anaemia,  more  particularly  those  forms  of  anaemia 
(such  as  chlorosis,  progressive  pernicious  anaemia,  etc.)  in 
which  there  is  defective  formation  of  blood,  is  the  chief  clinical 
condition  in  which  functional  endocardial  murmurs  occur. 
Now,  in  cases  of  this  description  the  muscular  fibre  of  the 
heart  becomes  fatty,  the  cardiac  cavities  become  dilated,  and 
the  weight  of  the  heart  also  becomes  increased  ;  in  fact,  there 
is  a  condition  of  combined  fatty  degeneration,  dilatation,  and 
hypertrophy,  dilatation  being,  however,  much  in  excess  of 
hypertrophy.^ 

Such  a  condition  of  the  heart  is  just  such  as  we  would 
expect  to  produce  '  relative  incompetence  ; '  and,  as  a  matter 
of  fact,  all  careful  clinical  observers  are,  I  presume,  agreed 
that,  in  cases  of  this  description,  mitral  and  tricuspid 
regurgitation  do  ultimately  occur.  yMl  observers  are  also,  I 
suppose,  at  one  in  thinking  that  arterial  murmurs  (pulmonary 
and  aortic    murmurs)  are   usually  present  in   advanced  condi- 

'  These  changes  are  seen  in  the  human  subject  in  cases  of  progressive  pernicious 
ansmia  ;  and  they  have  been  shown  by  Beau  to  occur  in  the  IcAver  animals  alter 
venesection. 


Functional  Murninrs.  i8g 

tions  of  anaemia.  The  point  which  is  still  undecided,  and 
which  has  lately  given  rise  to  so  much  controversy,  is  the 
nature  and  significance  of  the  basic  murmur,  which  is  heard 
in  the  second  left  interspace,  in  the  earlier  stages  of  anaemia, 
Three  theories,  all  of  which  have  warm  supporters,  have  been 
advanced  to  account  for  the  condition,  viz. — 

1.  That  the  vucrniiir  is  piiluionary. — The  exact  manner  in 
which  the  murmur  is  supposed  to  be  produced  in  the  pulmo- 
nary artery,  has  not  been  very  clearly  defined  by  the  supporters 
of  this  view  ;  the  sudden  propulsion  of  a  large  blood  wave 
of  abnormal  (spanaemic)  composition  into  the  vessel,  which  is 
probably  in  some  cases  at  least  dilated,  seems  to  me  an 
efficient  cause  for  its  production.  We  know,  as  a  matter 
of  fact,  that  the  heart,  in  cases  of  chlorosis,  is  not  only  weak, 
but  that  it  is  unusually  irritable  ;  that  even  in  the  earlier 
stages  the  right  ventricle  is  to  some  extent  dilated  ;  and  that 
the  blood  is  markedly  altered  in  composition. 

2.  That  the  mnrniur  is  due  to  mitral  regurgitation,  and 
that  it  is  conducted  to  the  anterior  wall  of  the  chest  through 
the  dilated  appendix  of  the  left  auricle. — (Dr  George  Balfour's 
theory). 

3.  That  the  murmur  is  produeed  in  the  pulmonary  artery 
as  the  result  of  constriction  of  that  vessel  ;  the  constriction 
being  caused  by  the  pressure  of  the  dilated  left  auricle.- — 
(Dr  Russell's  theory.)  Dr  Russell  further  believes  that  the 
systolic  murmur  heard  in  the  second,  third,  and  fourth  left 
interspaces  in  the  later  stages  of  such  cases,  is  due  to  tricuspid 
regurgitation. 

Before  considering  the  arguments  for  and  against  these 
different  theories,  I  may  say  that  the  question  is  still  an  open 
one,  the  balance  of  evidence,  in  my  opinion,  being  in  favour 
of  the  first  or  pulmonary  view.  I  do  not  think,  for  the  reasons 
to  be  presently  given,  that  Dr  Balfour  has  conclusively  proved 
his  point,  on  the  contrary,  there  seem  to  me  to  be  grave 
objections  to  his  view,  and  I  do  not  see  that  anything  which 
has  as  yet  been  advanced,  conclusively  negatives  the  first  or 
purely  pulmonary  theory. 


IQO  Diseases  of  fJie  Heart. 

Dr  Balfour  s   Theory. 

The  facts  and  arguments  on  which  Dr  Balfour  bases  his 
theory,  and  the  facts  and  arguments  which  seem  to  be 
opposed  to  it  may  be  summarised  as  follows : — 

1.  {For.)  That  in  organic  diseases  of  the  mitral  valve  a 
systolic,  basic,  and  apparently  pulmonary  murmur  is  often 
present.     Admitted  that  this  is  so. 

2.  {For.)  That  this  supposed  pulmonary  murmur  is,  as 
Naunyn  was  the  first  to  suggest,  not  pulmonary  at  all,  but 
that  it  is  due  to  mitral  regurgitation,  and  is  conducted  to  the 
second  left  interspace  through  the  dilated  appendix  of  the  left 
auricle. 

{Against?)  While  granting  that,  if  the  appendix  of  the  left 
auricle  were  dilated  and  were  in  contact  with  the  chest  wall, 
the  systolic  murmur  of  mitral  regurgitation  would  probably 
be  conveyed  to  the  second  left  interspace  ;  and  that,  as  Dr 
Balfour  points  out,  Naunyn's  theory  has  been  accepted  a^ 
highly  probable  by  many  leading  Continental  authorities,  it 
must  be  allowed  that  it  has  not  been  accepted  as  conclusively 
proved,  more  especially  by  many  competent  British  observers. 
But  even  granting  that  it  is  true  for  some  cases  of  organic 
disease  {i.e.  granting  that  cases  of  mitral  regurgitation  do 
occur,  in  which  the  usual  symptoms  and  signs  of  that  con- 
dition, more  especially  a  systolic  murmur  audible  at  the  apex, 
are  present,  and  in  which  the  auricular  appendix  is  dilated 
and  is  in  contact  with  the  chest  wall),  it  by  no  means  follows 
mat  the  chlorotic  murmur  with  which  we  are  now  more  parti- 
cularly concerned  is  produced  in  the  same  manner. 

The  arguments  with  which  Naunyn  supports  his  theory 
are  these : — 

{a)  {For.)  That  the  murmur  has  its  point  of  maximum  in- 
tensity at  a  point  an  inch  and  a  half  to  the  left  of  the  sternum. 

{Against)  Speaking  for  myself,  I  have  in  several  cases 
of  anaemia  failed  to  satisfy  myself  that  the  position  of  the 
maximum  intensity  is  so  sharply  defined  as  Dr  Balfour's 
statements  seem  to  indicate.  The  murmur  has  seemed  to  me 
in  several  cases  quite  as  loud   half  an   inch  to  the  left  of  the 


Functional  Murmurs.  191 

sternum  as  over  the  so-called  auricular  area,  i.e  an  inch  and  a 
half  to  the  left  of  that  bone.  Hayden,  who  is  admitted  to 
be  a  trustworthy  observer,  goes  much  further  in  this  respect 
than  I  am  disposed  to  do,  for  he  states  that  the  murmur  is 
best  heard  at  midsternum. 

But  even  granting  that  the  point  of  maximum  intensity 
of  the  murmur,  in  cases  of  chlorosis,  is  in  the  position  which 
Dr  Balfour  describes,  it  does  not  seem  to  me  by  any  means 
to  prove  that  the  murmur  is  not  pulmonary.  In  the  first  place, 
Sibson  has  shown  that  '  in  the  large  majority  of  cases'  which 
he  examined,  'the  greater  part  (in  25  of  45  instances),  or  the 
whole  (in  14  of  45  instances),  of  the  artery,  bore  to  the  left  of 
the  sternum,  and  presented  itself  behind  the  upper  costal  car- 
tilages and  their  spaces  from  the  first  cartilage  to  the  third 
space  ;'^  and  further,  that  the  average  breadth  of  the  vessel  in 
Pirogoff' s  five  front  views  of  the  healthy  heart  was  an  inch  and 
a  quarter.^  I  see  nothing  improbable,  therefore,  in  a  pul- 
monary murmur  having  (in  many  cases)  its  point  of  maximum 
intensity  considerably  to  the  left  of  the  sternum. 

In  the  second  place,  there  seems  good  reason  to  suppose,  as 
Dr  Russell's  observations  seem  to  show,  that  in  consequence 
of  the  dilated  condition  of  the  heart  (of  the  right  ventricle 
more  especially)  the  relative  position  of  the  parts  is  some\vhat 
altered,  and  that  the  pulmonary  artery  may  be  displaced  for- 
wards, and  perhaps  somewhat  to  the  left  of  its  usual  position. 

(Jj)  {For.)  That  this  point  does  not  correspond  to  the 
origin  of  the  pulmonary  artery,  but  does  exactly  correspond 
to  the  spot  where  the  appendix  of  the  left  auricle  comes 
up  from  behind,  just  to  the  left  of  that  artery,  and  that  in 
cases  of  this  description  {i.e.  where  the  murmur  is  loudly  heard 
in  the  second  left  interspace)  the  appendix  of  the  left  auricle 
is  dilated,  and  is  closer  to  the  chest  and  therefore  nearer  to 
the  ear  than  usual. 

{Against^  It  is  not  proved  that  the  appendix  of  the  left 
auricle  is  dilated  in  cases  of  chlorosis  (with  which  we  are  at 
present  more  immediately  concerned).  On  the  contrary  there 
are,  as  we  shall  presently  see,  positive  observations   to   the 

'   Russell  V^Gyx\o\A\  System  of  Mediciite,  vol.  iv.  p.  35.  "   //'.  p.   115. 


192  Diseases  of  the  Heart. 

contrary  ;  and  there  are,  as  Dr  Russell  has  pointed  out,  grave 
anatomical  objections  to  the  theory  that  the  left  auricular 
appendix  is  in  closer  contact  with  the  chest  wall,  in  cases  of 
chlorosis,  than  in  health.     This  point  will  be  again  referred  to. 

But  granting  for  the  moment  that  cases  of  mitral  regurgita- 
tion do  occur,  in  which  the  left  auricular  appendix  is  dilated, 
and  in  closer  contact  to  the  chest  wall  than  usual,  and  in  which 
the  systolic  murmur  produced  at  the  mitral  valve  is  heard  as 
loudly  in  the  second  left  interspace  as  at  the  apex,  that  is  no 
reason  for  supposing  that  in  a  case  of  anaemia, — in  which  a 
murmur  is  heard  in  the  second  left  interspace,  and  in  which 
there  is  no  murmur,  be  it  observed,  at  the  apex,  and  no  other 
indication  of  mitral  regurgitation  present, — this  apparently 
pulmonary  murmur  is  of  mitral  origin. 

The  fact  that  the  murmur  is  better  heard  over  the  auricular 
area  than  over  the  apex — the  normal  position  of  maximum 
intensity  for  mitral  murmurs — Naunyn  explains  by  attributing 
it  to  the  better  conduction  of  the  murmur  along  the  course 
of  the  regurgitating  blood  current,  the  fluid  veins  producing 
sonorous  vibrations  louder  at  the  point  of  impingement  than 
at  that  of  origin,  a  view  which  is  adopted  and  endorsed  by  Dr 
Balfour  in  support  of  his  theory.  He  says,  'the  fluid  veins 
formed  in  the  early  stage  of  chlorotic  regurgitation  are  of  low 
tension  and  but  little  force,  hence  the  vibrations  they  originate 
are  but  slightly  propagated  to  the  left  ventricle,  and  only  with 
difficulty  from  it  to  the  chest  wall  in  the  mitral  area,  where 
they  are  heard  as  an  impure  first  sound.  But  on  the  other 
hand  these  vibrations  are  readily  communicated  to  the  wall 
of  the  auricle  on  which  these  fluid  veins  impinge,  and  are 
easily  transmitted  to  the  chest  wall  with  which  the  auricular 
appendix  is  in  contact,  becoming  audible  in  the  auricular  area 
as  a  distinct  murmur.'^ 

Against  this  view  it  may  be  argued  that  if  the  fluid  veins 
produce  sonorous  vibrations  louder  at  their  point  of  impinge- 
ment than  at  their  point  of  origin  in  one  case,  why  should 
they  not  do  so  in  all .-'  In  other  words,  if  this  theory  be  cor- 
rect, we  ought  to  hear  the  systolic  murmur  of  organic  mitral 

'  Diseases  of  tlic  Heart.,  p.  177. 


Functional  Alurmurs.  193 

regurgitation  much  more  frequently  and  much  more  loudly  in 
the  second  left  interspace  than  is  admitted  by  the  majority  of 
British  observers,  at  all  events. 

Again,  it  may  be  asked  if  this  explanation  is  correct-  in 
cases  of  chlorosis,  and  if,  as  Dr  Balfour  admits,  '  the  auricle, 
at  the  moment  of  ventricular  systole,  is  not  only  full,  but 
somewhat  tense  from  unusual  dilatation,'  and  if  the  fluid  veins 
produce  sonorous  vibrations  louder  at  their  point  of  impinge- 
ment than  at  their  point  of  origin,  why  is  it  that  the  murmur  is 
not  heard  in  the  back,  under  the  left  scapula,  as  the  murmur 
of  organic  regurgitation  so  often  is  ? 

3.  {For.)  That  in  some  cases  of  mitral  disease, the  apparently 
pulmonary,  but  in  reality  auricular  murmur,  is  occasionally 
actually  louder  than  that  audible  in  the  mitral  area,  and  that  the 
murmur  of  mitral  regurgitation  is  sometimes  only  to  be  heard 
in  the  first  named  situation,  i.e.  in  the  second  left  interspace. 
Dr  Balfour  indeed  goes  so  far  as  to  state  that  '  a  more  or  less 
distinct  murmur  in  this  {i.e.  the  auricular)  area,  is  one  of  the 
earliest  indications  of  mitral  regurgitation  from  whatever 
cause. '^ 

{Against.)  While  admitting  that  some  authorities,  Rosen- 
stein  for  example,  support  this  view,  it  is  certainly  contrary 
to  the  recorded  opinion  of  almost  all  the  best  observers 
in  this  country,  and  I  am  not  prepared  to  admit  that  a 
systolic  murmur  heard  in  the  second  left  interspace  is,  per  se 
(as  Dr  Balfour  states  in  the  following  passage),  indicative  of 
mitral  regurgitation. 

'  In  chlorosis,'  says  Dr  Balfour,  '  in  which  all  these  pheno- 
mena, to  which  I  may  now  comprehensively  refer  under  the 
head  of  cardiac  dilatation  consecutive  to  spansemia,  exist  only 
in  the  very  slightest  degree,  this  pulmonary  or  rather  auricular 
murmur  is  always  present,  and  is  often — so  often  as  to  consti- 
tute it  almost  invariably —  the  sole  sign  of  mitral  regurgitation 
in  these  cases.'- 

4.  {For.)  Dr  Balfour  claims  'that  Naunyn's  view  is  even 
more  applicable  in  chlorosis  than  in  any  other  form  of  heart 
affection,   because    the    essential    cardiac    lesion    in    chlorosis 

'  Diseases  of  the  Heart,  second  edition,  p.  163.       -   //'/(/.  p.  172. 
N 


194  Diseases  of  the  Heart. 

is  muscular  relaxation  and  progressive  dilatation,  hence  at  a 
comparatively  early  stage  of  the  disease  the  dilated  right 
ventricle  has  separated  the  left  ventricle  from  the  chest  wall, 
while  the  dilated  appendix  of  the  left  auricle  has  been  pari 
passu  brought  into  closer  contact  with  it.'  ^ 

'  The  peculiar  position  of  the  murmur  is  due,'  says  Dr 
Balfour,  '  to  the  altered  position  of  the  heart.  '  This  is  due  to 
the  dilatation  of  the  right  ventricle,  which  dilates  pari  passu 
with  the  left  ventricle,  and,  like  a  water  cushion,  separates  it 
from  the  chest  wall,  leaving  the  dilated  appendix  of  the  left 
auricle  the  only  part  of  the  left  side  of  the  heart  in  contact 
with  the  chest  wall.'  - 

Dr  Balfour  further  claims  that  the  pulsation  of  the  auri- 
cular appendix  can  be  seen,  felt,  and  graphically  recorded  by 
the  cardiograph.  He  says — '  In  this  situation,  the  dilated 
appendix  not  infrequently  gives  rise  to  so  distinct  a  pulsation 
that  its  movements  can  be  traced  by  the  cardiograph,  and  the 
history  of  several  such  cases  has  been  published,  and  their  car- 
diograms figured  by  my  former  resident,  Dr  George  Gibson, 
while  the  pulsation  is  so  well  marked  and  forcible  in  some  of 
these  cases,  that  the  late  Dr  Hughes  Bennett  sent  me  on  one 
occasion  a  case  of  chlorosis  as  a  case  of  aortic  aneurism.'  ^ 

Against  these  statements  it  may  be  argued  firstly,  that 
Naunyn's  explanation  seems  more  particularly  to  apply  to  those 
cases  of  mitral  regurgitation  in  which  a  systolic  murmur  is 
audible  at  the  apex,  i.e.  in  the  usual  mitral  area,  as  welt  as  in 
the  second  left  interspace  ;  but  that  in  the  earlier  stages  ot 
chlorosis,  the  apparently  pulmonary  murmur  is,  as  Dr  Balfour 
himself  admits,  usually  the  sole  sign  of  mitral  regurgitation  ; 
in  other  words,  the  usual  evidence  of  mitral  regurgitation,  i.e  , 
a  systolic  murmur  in  the  mitral  area,  is  wanting. 

Secondly,  that  in  the  later  stages  of  anaemia  (chlorosis)  a 
true  mitral  murmur,  i.e.  a  murmur  audible  at  the  apex — in 
the  mitral  area — does  actually  occur.  This  Dr  Balfour  him- 
self admits,  and  he  explains  it  in  the  following  manner:  — 

'  Diseases  of  the  Heart,  second  edition,  p.  176. 
-  Edinburgh  Medical  Joiirital,  Oct.  18S2,  p.  295. 
^  Diseases  of  the  Heart,  p.  175. 


Functional  Murnuirs.  195 

'  By  and  by,  as  the  regurgitation  increases,  and  the  ventricle 
hypertrophies,  these  fluid  veins  gain  force  sufficient  to  be  com- 
municated through  the  ventricle  also,  hence  in  the  later  stages 
of  chlorosis  we  have  a  mitral  murmur  associated  with  the 
auricular  one.  It  is  however  quite  possible  that  this  murmur 
in  the  mitral  area  is  really  tricuspid,  due  to  the  increased 
dilatation  of  the  right  ventricle,  the  apex  of  which  may  even 
occupy  the  mitral  area ;  this  not  infrequently  occurs  in 
mitral  stenosis,  it  is  not  an  improbable  event  in  chlorosis, 
and  it  is  of  little  consequence  which  explanation  we  accept, 
the  actual  truth  probably  embracing  both  conclusions,  being 
sometimes  due  to  the  one  cause  and  sometimes  to  the  other.'  ^ 

Now  I  agree  with  Dr  Balfour  in  thinking  that  in  many 
cases  of  advanced  chlorosis  the  systolic  murmur,  which  is 
heard  at  the  apex,  is  due  to  mitral  regurgitation,  but  I  differ 
from  him  in  as  much  as  I  believe  that  it  is  a  distinct  murmur 
from  that  heard  in  the  second  left  interspace  ;  and  I  am 
unable  to  accept  the  theory  which  he  advances  to  explain  the 
supposed  fact  that  a  mitral  murmur  may,  in  the  earlier  stages 
of  the  condition  be  confined  to  the  base,  while  in  the  later 
stages  it  is  heard  at  the  apex.  For  is  it  not  the  fact  that  as 
cases  of  chlorosis  (and  more  especially  of  progressive  per- 
nicious anaemia,  in  which  the  same  sequence  of  events  occurs), 
advance,  that  the  degeneration  of  the  heart  muscle  increases, 
and  that  dilatation  of  the  heart  cavities,  with  increased  feeble- 
ness of  action,  rather  than  hypertrophy  with  increased  force 
of  contraction,  occurs  ?  If  this  is  so,  Dr  Balfour's  explanation 
obviously  cannot  hold  good  ;  and  he  himself  states  that  '  the 
essential  cardiac  lesion  in  chlorosis  is  muscular  relaxation  and 
progressive  dilatation.'^ 

The  order  of  recovery,  too,  seems  to  be  opposed  to  this 
view.  If  the  hypertrophy  of  the  left  ventricle  is  the  cause  of 
the  mitral  murmur  being  audible  at  the  apex  in  advanced 
stages  of  the  case,  and  if  the  mitral  and  so-called  auricular 
murmurs  depend  on  one  and  the  same  cause,  i.e.  upon  mitral 
regurgitation,  why,  in  cases  which  recover,  should  the  basic 
murmur  persist  long  after  the  apex  murmur  has  disappeared  .-" 

'  Diseases  of  tlie  Heart,  second  edition,  p.   177.  -  Ibid.  p.  176. 


196  Diseases  of  the  Heart. 

It  can  hardly  be  suggested  that  the  left  ventricle  becomes 
weaker  during  the  process  of  recovery ;  and  if  both  murmurs 
depend  on  one  and  the  same  cause,  i.e.  upon  mitral  regurgi- 
tation, and  if  the  ventricle  does  not  become  weaker,  both  mur- 
murs, surely,  ought  to  disappear  at  one  and  the  same  time. 

Tliirdly,  Dr  Russell  has  shown  that  in  a  case  of  pro- 
gressive pernicious  anaemia,  in  which  both  pulsation  and 
bruit  were  present  in  the  second  left  interspace  during  life, 
the  auricular  appendix  was  not  dilated,  and  was  not  in  contact 
with,  but  was  far  removed  from,  the  chest  wall,  and  that  the 
pulsation,  pcrcussion-dulness  and  bruit  were  respectively  seen 
and  heard  over  the  conus  arteriosus.^ 

Dr  Balfour's  counter  argument  against  this,  '  that  the 
position  of  the  auricle  post-viortevi  is  no  proof  of  its  state 
during  life,  and  where  there  is  no  mitral  stenosis,  an  auricular 
appendix  beating  in  the  second  interspace  during  life,  may 
very  well  empty  itself  and  contract  out  of  sight  in  the  act  of 
dying,'  ^  is  not,  to  my  mind,  a  very  convincing  one.  In  the 
first  place,  our  knowledge  of  the  normal  position  of  the 
appendix  (including  Naunyn's  own  observations,  which  Dr 
Balfour  quotes  as  one  of  his  main  arguments),  has  been 
largely  acquired  by  the  same  means  which  were  adopted  in 
this  case.  And  in  the  second  place,  in  cases  of  progressive 
pernicious  anaemia,  such  as  this  was,  the  heart  is  usually  (I 
think  I  may  say  invariably)  relaxed  and  flaccid  after  death. 
It  seems  unlikely,  therefore,  that  in  this  case  the  appendix 
emptied  itself  and  contracted  out  of  sight. 

Fourthly,  That  when  the  right  cavities  of  the  heart  are 
dilated,  as  Dr  Balfour  admits  is  the  case,  in  chlorosis — the 
condition  we  are  considering — the  left  auricular  appendix  is 
usually  quite  invisible  from  the  front,  a  fact  which  Dr  Russell 
has  also  urged.  I  have  had  several  opportunities  of  verifying 
this  statement  during  the  past  year,  two  of  the  cases  being 
typical  examples  of  pernicious  anaemia.  In  none  of  these 
cases  was  the  appendix  much  dilated,  indeed  in  one  of  the 
cases  of  pernicious  anaemia  it  was  considerably  smaller  than 
usual.     Dr  Russell  says  —  'It  is  further  recognised   that,  in 

'  Edinr.  Medical Joiinial,  Nov.  1S82,  p.  408.         -  Ibid.  Sept.  1S82,  p.  197. 


Functional  Murmurs.  197 

debility,  owing  to  dilatation  of  the  right  ventricle,  the  left  is 
displaced  outwards  and  backwards ;  or  a  change  occurs 
which  may  be  regarded  as  a  rotatory  movement  of  the  heart 
round  its  longitudinal  axis  ;  and  this  must  be  conceded  as 
having  a  displacing  effect  on  the  auricle  analogous  to  what  it 
has  on  the  ventricle  of  the  same  side.'  Further,  Dr  Russell 
argues  that,  since  '  the  origin  or  root  of  the  appendix  is 
overlapped  in  part  by  the  pulmonary  artery,  so  to  reach  the 
parietes  the  appendix  has  to  traverse  a  course  equal  to  the 
diameter  of  that  vessel.  Any  increase  in  the  diameter  of  the 
artery,  from  increase  of  its  contents  will  thus  place  the 
appendix  deeper  in  the  chest.'  ^ 

I  can  from  personal  observation  testify,  as  Dr  Russell's 
argument  implies,  that  the  pulmonary  artery  is  dilated  in 
(some)  cases  of  pernicious  ansemia,  presumably  therefore  it  is 
dilated  in  some  cases  of  chlorosis. 

It  must  be  at  once  conceded  that  pulsation  is  frequently  to 
be  observed  in  the  second  left  interspace  in  cases  of  chlorosis. 
I  cannot,  however,  say  that  I  have  ever  been  able  to  satisfy 
myself  that  it  was  auricular  ;  and,  like  Dr  Broadbent,  I  am 
not  at  all  convinced  that  Dr  Gibson's  latter  tracings,  to  which 
Dr  Balfour  particularly  refers  (see  Edijiburgh  Medical  jfoiirnal, 
October  1882,  p.  294),  prove  the  pulsation  to  be  produced  by 
regurgitation  into  the  ventricle  from  the  auricle.  The  tracings 
published  by  Dr  Russell  in  the  British  Medical  Journal  of 
June  2,  1882,  seem  also  opposed  to  Dr  Gibson's  view. 

Further,  in  common  with  Dr  Broadbent,  Dr  Goodhart, 
Dr  Russell  and  other  observers,  whose  pathological  experi- 
ence is  not  inconsiderable,  I  have  not  met  with  any  case  of 
cardiac  dilatation — certainly  not  any  case  of  anaemia,  and  I 
have  had  an  opportunity  of  examining  seven  or  eight  cases, 
after  death — in  which  the  left  auricular  appendix  was  so 
markedly  dilated  '  as  to  warrant  the  belief  that  it  could  have 
been  the  cause  of  the  extensive  pulsation  claimed  for  it  by 
Dr  Balfour  in  the  second  and  third  left  spaces.' 

Again,  Dr  Russell  claims  to  have  frequently  satisfied 
himself  that  the  pulsation  in  the  second  interspace  in  cases 

'  Edinr.  Med.  Jour.,  Aug.  1882,  p.  131.     "  Brit.  Mcd.Jo-tir.,  Aug.  26,  1882,  p.  354. 


1 98  Diseases  of  the  Heart. 

of  oi'Gfanic  mitral  disease,  is  due  to  the  dilated  ri<:^ht  ventricle. 
I  can  corroborate  Dr  Russell's  statement  in  this  respect, 
inasmuch  as  I  have  in  several  cases  of  right-sided  dilatation — 
notably  in  a  case  of  pernicious  annemia — found  that  a  needle 
passed  into  the  second  left  interspace  transfixed  the  conus 
arteriosus  of  the  right  ventricle,  and  did  not  transfix  the 
pulmonary  artery,  as  it  does  under  normal  circumstances. 

To  the  other  points  previously  advanced  in  support  of  and 
against  Dr  Balfour's  theory,  the  following  must  be  added  : — 

5.  {For.)    That  the  pulmonary  second  sound  is  accentuated. 

We  all,  of  course,  know,  that  in  mitral  regurgitation,  the 
pulmonary  second  sound  is  accentuated  in  consequence  of  the 
increased  blood-pressure  in  the  pulmonary  artery,  which  results 
from  the  mitral  lesion.  If,  therefore,  the  accentuation  occurs 
in  the  earlier  stages  of  chlorosis,  and  if  it  cannot  be  satisfac- 
torily accounted  for  in  any  other  manner  (than  as  the  result 
of  mitral  regurgitation),  we  must  of  course  admit  that  it  is 
strongly  corroborative  of  Dr  Balfour's  theory,  always  pre- 
mising that  there  is  no  fatal  objection  to  that  view. 

{Against.)  Now,  I  at  once  admit  that,  in  the  later  stages  of 
ansemia,  the  pulmonary  second  sound  is  often  intensified,  and 
that  the  accentuation  may  be  due  to  the  mitral  regurgitation 
which  is  often  present  in  the  advanced  stages  of  that  condition. 
In  the  earlier  stages  of  chlorosis,  too,  I  have  frequently  (though 
not  invariably)  found  the  pulmonary  second  sound  louder 
than  the  aortic.  I  have  been  in  the  habit  of  regarding  the 
accentuation,  which  occurs  in  the  early  stages  of  chlorosis,  as 
apparent  rather  than  real  ;  in  other  words,  I  have  supposed 
that  the  aortic  second  sound  was  diminished  in  intensity, 
while  the  pulmonary  retained  its  normal  loudness.  Possibly 
I  may  have  been  mistaken  in  this  view,  for  the  fact  that  the 
blood  pressure  in  the  peripheral  arteries  is  increased  rather 
than  diminished  in  anaemia,  would  probably  lead  to  accen- 
tuation rather  than  diminution  of  the  aortic  second  sound  ;^  and 

'  It  is  well  established  that  the  blood-pressure  is  increased  in  the  earlier  stages 
of  anaemia.  The  increase  is,  I  believe,  due  to  two  causes  viz.,  (a)  increased 
adhesions  of  the  red  corpuscles  to  the  capillary  walls,  (/')  contraction  of  the  peri- 
pheral blood  vessels,  the  result  of  anaemia  of  the  vaso-motor  centre. 


Functional  Mni'murs.  199 

I  am  certainly  not  prepared  to  say  that  true  accentuation 
of  the  puhnonary  second  sound  does  not  occur,  even  in  the 
earHer  stages  of  chlorosis. 

But  even  granting  that  the  accentuation  were  always 
present  and  well  marked,  I  cannot  admit  that  it  is  suffi- 
ciently strong  evidence  to  counterbalance  the  grave  objections 
which  have  been  advanced  against  the  mitral  regurgitation 
view.  In  particular,  the  objections  which  Dr  Russell  has  so 
ably  urged,  and  which  I  can  not  only  corroborate  but  also 
strengthen,  viz.: — (i)  that  in  the  most  advanced  stages  of 
anaemia,  as  seen  after  death,  the  left  auricle  appendix  is  not 
dilated  (in  one  of  my  cases  it  was  actually  smaller  than 
normal) ;  and  (2)  that  when  the  right  heart  becomes  dilated, 
as  it  does  in  conditions  of  anaemia,  the  appendix  of  the  left 
auricle  recedes  from,  rather  than  comes  in  closer  contact  with 
the  chest-wall — seem  to  me  to  negative  Dr  Balfour's  view. 
I  feel  obliged,  therefore,  to  suppose,  that  if  the  pulmonary 
second  sound  is  actually  intensified,  the  accentuation  must  be 
due  to  some  other  cause  than  mitral  regurgitation.  One 
cause  of  the  accentuation  is,  I  believe,  the  diminished  suction 
power  which  the  left  ventricle  exerts  in  consequence  of  the 
relaxed  and  feeble  condition  of  its  muscular  wall ;  the  flow  of 
blood  from  the  lungs  to  the  left  heart  is  not  facilitated  (on  the 
occurrence  of  the  ventricular  diastole)  as  it  is  in  health.  An- 
other cause  may  possibly  be  found  in  the  altered  composition 
of  the  blood,  though  this  is,  to  say  the  least,  extremely  doubt- 
ful. Dr  Gaskell,  indeed,  whom  I  consulted  on  this  matter,  is 
inclined  to  think  that  a  diminished  number  of  blood  corpuscles 
would  facilitate  rather  than  retard  the  flow  of  blood  through 
the  lungs;  he  writes — '  As  to  your  question  about  the  passage 
of  the  blood  through  the  lungs  in  anaemia,  I  should  think  that 
probably  the  blood  would  pass  through  more  easily  for  one 
reason  at  all  events  ;  the  experiments  of  Ewald  (Archiv.  f.  Anat. 
u  Physiologic  1877,  ueber  die  Transpiration  des  Blutes)  have 
shown  that  defibrinated  blood  passes  through  fine  capillaryglass 
tubes  much  more  easily  when  there  are  few  or  no  corpuscles 
in  it  than  in  the  normal  condition,  so,  for  this  reason  alone, 
the  blood-flow  should  be  more  easy.     On  the  other  hand,  the 


200  Diseases  of  the  Heart. 

anaemic  condition  of  the  blood  would  probably  excite  the 
vasomotor  centre,  and  so  tend  to  constrict  the  blood  vessels 
of  different  vascular  areas,  and  therefore  increase  arterial  pres- 
sure. There  is,  however,  no  necessity  that  the  pulmonary 
vessels  should  take  part  in  such  constriction,  and,  indeed,  the 
evidence  points  rather  the  other  way,  for  excitation  of  the 
vasomotor  centre,  either  directly  or  reflexh',  by  means  of 
the  stimulation  of  a  sensor>^  nerve,  does  not  appear  to 
diminish  but  rather  to  increase  the  flow  of  blood  through  the 
lungs,  and  similarly,  I  should  imagine,  that  in  the  case  of  any 
excitation  of  the  vasomotor  centre,  through  an  anaemic  con- 
dition of  the  blood,  no  constriction  of  the  pulmonary  vessels 
would  take  place,  but  if  anything  dilation.  For  both  reasons, 
therefore,  it  is  more  likely  than  not  that  the  passage  of 
the  blood  through  the  lung  vessels  takes  place  with  greater 
facility  when  there  are  fewer  red  blood  corpuscles.' 

Dv  Rnsscirs  Theory. 

Let  us  now  turn  to  Dr  Russell's  theory.     He  believes  : — 

(i)  That  the  murmur  heard  in  the  second  left  interspace, 
in  the  earlier  stages  of  chlorosis,  is  generated  in  the  pulmo- 
nary artery. 

(2)  That  the  murmur  is  due  to  a  relative  constriction 
of  the  vessel  {i.e.  of  the  pulmonary  artery),  produced 
by  the  pressure  of  the  dilated  left  auricle,  which  is  situated 
behind  it. 

Now  this  theory  necessarily  presupposes  that,  during  the 
ventricular  systole,  the  pressure  of  the  blood  in  the  left  auricle 
is  greater  than  the  pressure  of  the  blood  in  the  pulmonary 
artery;  for  otherwise  the  pulmonary  artery  could  not,  of  course, 
be  constricted  by  the  pressure  of  the  auricle.  That  this  is  so 
Dr  Russell  maintains  ;  and  he  contends  that  the  excessive 
pressure  (if  I  may  so  term  it)  in  the  left  auricle  is  due  to  a 
regurgitant  current  being  propelled  into  it  (the  left  auricle), 
by  the  left  ventricle  through  the  mitral  orifice. 

The  explanation  which  he  gives  is  as  follows  : — '  Owing 
to  the  tension  in  the  pulmonary  vessels,  the  fulness  of  the 
auricle    must    at    all    times    be   increased  ;  in  fact,  the  blood 


Fiinctional  Mttrmtirs.  201 

coming  from  the  lungs  pours  into  it  as  rapidly  as  it  empties 
itself  into  the  ventricle,  the  result  being  that  its  cavity,  al- 
though enlarged  by  sharing  in  the  debilitating  influences  in 
existence,  is  already  full  before  the  ventricular  systole  not 
only  prevents  further  relief  to  the  tension  in  the  pulmonary 
circuit,  but  throws  back  upon  it  (the  auricle)  the  blood 
embraced  by  the  segments  of  the  mitral  valve  as  they  swing 
to  close  the  auriculo-ventricular  orifice,  as  well  as  the  column 
of  regurgitant  blood  from  the  ventricle.'  ^  And  again,  '  The 
question,  then,  arises  as  to  what  force  may  act  through  the  left 
auricle,  and  is  it  greater  than  that  of  the  right  ventricle  ? 
Take  mitral  regurgitation  :  there  a  stream,  at  times  of  con- 
siderable magnitude,  passes  back  into  the  auricle  with  all  the 
force  exerted  by  the  systole  of  the  left  ventricle  ;  and,  as  we 
cannot  assume  the  left  auricle  to  be  a  vacuum  ready  to  receive 
this  regurgitating  stream,  there  must  be  a  backward  flow 
through  it,  nearly  as  much  greater  in  force  than  the  flow  in 
the  pulmonary  artery  as  the  systole  of  the  left  ventricle  is 
greater  than  the  right.  .  .  .  The  next  question  to  consider 
is,  whether  the  tension  in  the  left  auricle  is  greater  than  that 
in  the  pulmonary  artery  at  the  moment  of  ventricular  systole.'- 
.  .  .  '  When  it  is  remembered  that  there  is  not  only  a  column 
of  blood  sent  with  the  force  of  the  left  ventricle  into  this  tense 
auricle,  but  also  that  the  mitral  cusps,  instead  of  being  held 
well  down  into  the  ventricle  and  presenting  a  concavity 
towards  the  auricle,  so  as  thereby  to  relieve  the  auricle  and 
'  make  room  for  the  returning  blood  without  hindrance,'  must, 
on  the  contrary,  owing  to  the  enfeebled  state  of  the  papillary 
muscles,  be  allowed  greater  latitude  of  movement  towards  the 
auricle,  it  must  be  granted  that  the  auricular  tension  bears  a 
fixed  relation  to  the  strength  of  the  left  ventricle,  and  is  there- 
fore greater  than  that  in  the  pulmonary  artery.'^ 

In  opposition  to  this  theory  Dr  Balfour  maintains  that  '  it 
is  absolutely  impossible  that  the  left  auricle  can  ever  so  com- 
press the  pulmonary  artery  ; '  .  .  .  and  '  that  it  is  obviously 
impossible  that  the  circulation  could  be  carried  on  under  these 

'  Edinburgh  Medical  Journal,  Aug.  1882,  p.  134. 
*  Ibid.  Nov.  1882,  p.  411.        '  Ibid.  Nov.  1882,  p.  412. 


202  Diseases  of  the  Heart. 

conditions.'  It  is  unnecessary,  I  think,  to  detail  the  facts  and 
arguments  with  which  Dr  Balfour  supports  these  objections, 
and  the  facts  and  arguments  which  Dr  Russell  urges  in  reply, 
for  (granting  for  the  moment  that  Dr  Balfour's  objections  are 
invalid)  I  maintain  : — 

That  even  if  such  excessive  intra-auricular  pressure 
could  occur,  it  certainly  is  not  present  in  the  early  stages  of 
chlorosis — the  condition  which  we  are  now  considering.  Such 
excessive  intra-auricular  pressure  could  only  be  produced  by 
extremely  free  mitral  regurgitation.  In  all  cases  of  mitral 
regurgitation  there  is  probably  a  considerable  direct  obstacle 
(both  valvular  and  muscular),  in  addition  to  the  blood  pressure 
in  the  auricle,  opposed  to  the  force  of  the  left  ventricle  ;  while 
there  is  no  direct  obstacle,  but  only  the  blood-pressure  in  the 
pulmonary  artery,  opposed  to  the  force  of  the  right  ventricle. 
We  cannot,  therefore,  with  fairness  say,  because  the  left 
ventricle  is  much  stronger  than  the  right,  it  wall  in  mitral 
regurgitation  raise  the  blood  pressure  in  the  left  auricle  higher 
than  the  right  ventricle  will  raise  the  blood  pressure  in  the 
pulmonary  artery.  The  right  ventricle,  though  much  weaker, 
is  acting  (more  especially  when  the  tricuspid  is  sound)  at  an 
immense  advantage,  and  undoubtedly  propels  a  much  larger 
quantity  of  blood  into  the  pulmonary  artery  than  the  left 
ventricle  propels  (in  any  ordinary  case  of  mitral  regurgitation) 
into  the  left  auricle.^ 

Now,  there  is  not  sufficient  evidence,  I  maintain,  to  prove 
that  any  regurgitation  through  the  mitral  valve  occurs  in 
the  early  stages  of  chlorosis  and  anaemia,  much  less  the  free 
regurgitation,  which  would  be  required  to  produce  the  ex- 
cessive pressure  in  the  left  auricle,  which  Dr  Russell's  theory 
requires. 

The  only  evidence  which  Dr  Russell  produces  in  favour  of 
mitral  regurgitation  in  the  early  stages  of  chlorosis,  is  an  accen- 
tuated pulmonary  second  sound.  '  It  will  not  be  seriously 
denied  here,'  says  Dr  Russell,  '  that  in  these  affections  there  is 
a  relative  insufficiency  of  the   mitral   valve,  the  result  of   a 

'  The  reader  is  referred  to  the  original  papers.     See  the  Edinburgh  Medical 
Journal,  August  and  September  1SS2,  p.  19S  ;  and  November  1882,  p.  409. 


Functional  Afurmnrs.  203 

debilitated  and  relaxed  condition  of  the  cardiac  muscle,  in- 
cluding the  musculi  papillares.  This  insufificiency,  however, 
is  not  always  evidenced  by  a  bruit  at  the  apex,  the  point  at 
which  mitral  bruits  are  ordinarily  audible  ;  but  regurgitation 
is  assumed  ^  from  the  accentuation  of  the  pulmonary  second 
sound,  and  from  the  presence  of  a  systolic  murmur  in  the 
pulmonary  area.'  - 

1  have  already  given,  in  detail,  the  facts  and  arguments 
which  are,  I  consider,  opposed  to  Dr  Balfour's  view,  and  have 
previously  stated  that  the  presence  of  a  systolic  murmur  in 
the  second  left  interspace  is  not,  in  my  opinion,  per  se  (I 
may  add,  nor  when  conjoined  with  an  accentuated  pulmonary 
second  sound)  sufficient  evidence  of  mitral  regurgitation. 
And  Dr  Russell  himself  maintains  that  this  systolic  murmur 
is  in  reality  produced  in  the  pulmonary  artery.  According  to 
his  own  showing,  then,  the  only  evidence  of  mitral  regurgi- 
tation which  remains  is  accentuation  of  the  pulmonary  second 
sound.     This  I  maintain  is  insufficient  evidence. 

Since  this  lecture  was  written,  Dr  Russell  seems  to  have 
modified  the  view  which  he  originally  proposed,  inasmuch  as 
he  no  longer  insists  that  the  increased  tension  of  the  left 
auricle  (which  his  theory  necessarily  supposes  is  present  dur- 
ing the  first  part  of  the  ventricular  systole)  is  due  to  mitral 
regurgitation.  In  the  passage  quoted  in  the  foot-note,  from 
his  instructive  paper  in  the  BritisJi  Medical  Journal  oi  ]w\-\&  2d 
1883,  he  suggests  that  the  increased  tension  of  the  left  auricle 
may  be  due  to  the  incomplete  emptying  of  the  left  ventricle 
during  its  systole,  and  consequent  imperfect  relief  to  the  full 
auricle.^ 

But  if  this  view  be  correct,  should  we  not  expect  to  hear  a 

■  Dr  Russell  is  here  speaking  of  Dr  Balfour's  theory ;  he  himself  believes 
that  the  systolic  basic  murmur  is  not  mitral,  but  pulmonary, 

^  Edinburgh  Medical  Journal,  Aug.  1882,  p.  130. 

*  '  I  shall  now  endeavour  to  explain  the  clinical  phenomena.  The  accentuation 
of  the  pulmonary  second  sound,  if  no  lung  affection  be  present,  must  be  taken  as 
indicating  an  abnormal  accentuation  of  blood  behind  the  mitral  orifice.  Whether 
this  be  due  to  the  incomplete  emptying  of  the  left  ventricle  during  its  weakened 
systole,  and  consequent  imperfect  relief  to  the  full  auricle,  or,  from  the  first,  due 
to  a  certain  amount  of  regurgitation,  or  to  both  these  causes,  it  is  unnecessary  to 


204  Diseases  of  the  Heart. 

systolic  pulmonary  murmur  as  a  necessary  accompaniment  of 
all  cases  of  organic  mitral  disease,  in  which  the  pulmonary 
second  sound  is  accentuated  ?  We  can  hardly  suppose  that 
the  distention  of  the  left  auricle  is  great  in  the  early  stages  of 
chlorosis  ;  and  if  a  small  amount  of  distention  is  sufficient 
to  constrict  the  pulmonary  artery,  and  to  produce  a  systolic 
murmur,  should  we  not  a  fortiori  expect  to  have  a  sys- 
tolic pulmonary  murmur  produced  in  those  cases  of  mitral 
stenosis,  for  example,  in  which  we  may  legitimately  con- 
clude that  the  distention  of  the  auricle  is  still  more  con- 
siderable ?  It  may,  of  course,  be  argued  (i)  that  a  systolic 
murmur  is  sometimes  heard  in  the  pulmonary  area  in  cases  of 
mitral  stenosis  ;  and  (2)  that  in  those  cases  of  mitral  stenosis 
in  which  a  systolic  pulmonary  murmur  is  not  present,  the  left 
auricle  is  not  dilated.  In  support  of  the  latter  proposition,  it 
may  be  urged  that  in  mitral  stenosis  the  cardiac  muscle  is 
not  degenerated,  as  it  is  in  the  case  of  anaemia,  and  that  the 
left  auricle,  for  a  time  at  all  events,  is  able  to  resist  the  exces- 
sive blood-pressure  in  its  interior,  and  does  not  dilate.  But 
looking  at  the  matter  from  the  broad  ground  of  clinical 
experience,  most  observ'ers  will,  I  think,  agree  that  cases 
(such  as  mitral  stenosis,  mitral  regurgitation,  fatty  heart,  etc.), 
are  frequently  met  with,  in  which  the  left  auricle  is  quite 
as  much  distended  as  we  can  legitimately  suppose  it  to  be 
in  the  earlier  stages  of  chlorosis,  and  in  which  there  is  no 
pulmonary  systolic  murmur.  If  this  general  proposition  be 
granted,  we  must  of  course  conclude  that  the  pulmonary 
murmur,  met  with  in  the  earlier  stages  of  chlorosis,  is  not 
produced  by  the  pressure  of  the  distended  left  auricle  upon 
the  pulmonary  artery,  but  that  it  is  due  (either  wholly  or  in 
part)  to  some  other  condition  or  conditions. 

I   feel    obliged,   therefore,    to    dissent    from    Dr    Russell's 
theory ;  and    there    are    (as    I    have    already  pointed   out    in 

discuss  here.  The  fact  of  accumulation  of  blood  in  the  pulmonan-  circuit,  includ- 
ing the  left  auricle,  is  sufficient  for  our  present  purpose,  and  is  warranted  by  the 
evidence  given  by  pulsation  at  the  root  of  the  neck,  by  the  course  of  the  external 
jugulars  becoming  \nsible,  and  perhaps  by  pulsation  appearing  over  the  right 
ventricle,  that  a  like  accumulation  is  taking  place  in  the  right  chambers  of  the 
heart  and  the  large  vessels  leading  to  it.' 


Functional  Murmurs.  205 

detail),  in  my  opinion,  grave  objections  to  Dr  Balfour's  view. 
I  am  compelled,  therefore,  by  the  method  of  exclusion,  to  fall 
back  upon  the  purely  pulmonary  theory,  and  to  ask  whether 
there  is  any  conclusive  reason  why  the  murmur  should  not  be 
generated  in  the  pulmonary  artery  itself,  irrespective  of  any 
constriction  by  the  pressure  of  the  auricle,  such  as  Dr  Russell's 
theory  implies.^ 

The  Purely  Pulmonary  Theory. 

Dr    Balfour    argues    that    the    murmur    cannot    be    pul- 
monary ;  — 

(i.)  Because  '  there  are — in  chlorosis — no  causes  of  murmur 
operative  at  the  pulmonary  orifice  which  are  not  at  least  as 
active  at  the  aortic  opening,  so  that  a  pulmonary  murmur 
would  certainly  be  accompanied  by  an  aortic  murmur  also, 
and  the  latter  would,  of  course,  be  propagated  along  the 
course  of  the  aorta,  and  more  or  less  distinctly  into  the 
carotids.'^  This  argument  does  not,  however,  appear  to  be 
conclusive.  In  the  first  place,  we  might  as  well  say,  in  oppo- 
sition to  Dr  Balfour's  own  view — the  auricular  theory- — that 
the  murmur  cannot  be  mitral,  because  there  are  no  causes  of 
murmur  operative  at  the  mitral  orifice,  which  are  not  at  least 
as  active  at  the  tricuspid  opening,  so  that  a  mitral  murmur 
would  certainly  be  accompanied  by  a  tricuspid  murmur  ;  and 
since  it  is  generally  admitted,  and  as  Dr  Balfour  himself 
allows  in  the  passage  quoted  below,  that  the  tricuspid  mur- 
mur is  of  later  occurrence  than  the  mitral  murmur,  Dr 
Balfour's  auricular  theory  falls  to  the  ground.  Dr  Balfour 
says,  '  shortly  after  the  appearance  of  the  primary  haemic 
murmur,  a  tricuspid  murmur  and  jugular  undulation  are 
found  to  be  developed.     This  is  naturally  accompanied  by  a 

'  There  seems  to  me  to  be  no  sufficient  evidence  to  justify  the  belief,  that  the 
murmur  heard  in  the  second  left  interspace,  hi  the  ea?-ly  stages  of  ancemia,  is  due 
to  tricuspid  regurgitation,  as  Parrot  supposed.  The  mere  presence  of  a  murmur 
in  that  position,  in  the  absence  of  the  usual  signs  of  tricuspid  regurgitation,  is 
insufficient  evidence  to  justify  such  a  belief.  It  is,  however,  quite  possible  that, 
in  the  later  stages  of  anaemia,  a  tricuspid  murmur  ma}'  be  heard  in  this  situation,  as 
Dr  Russell  supposes. 

^  Edinburgh  Medical  Journal,  Oct.  1882,  p.  294. 


2o6  Diseases  of  the  Heart. 

pulmonary  and  also  by  an  aortic  systolic  murmur  the 
active  cause  in  the  production  of  both  these  murmurs  being 
the  large  blood-waves  sent  on  by  the  dilated  and  hypertro- 
phied  ventricles,  as  was  first,  I  believe,  pointed  out  by  Beau.'^ 

In  the  second  place,  I  am  not  prepared  to  admit,  uncon- 
ditionally, that  there  are  no  causes  of  murmur  operative  at  the 
pulmonary  orifice,  which  are  not  at  least  as  active  at  the 
aortic  orifice.  It  appears  to  me  quite  possible  that  such 
causes  may  exist  in  the  respective  conditions  of  the  two  ven- 
tricles ;  in  the  respective  resistances  which  the  arterial  blood 
meets  with  at  the  orifice  of  the  aorta  and  in  the  systemic 
circulation,  and  which  the  venous  blood  meets  with  at  the 
orifice  of  the  pulmonary  artery  and  in  its  passage  through 
the  lungs  ;  and  in  the  respective  physical  conditions  (calibre, 
thickness  of  coat,  relationship  to  the  chest  wall,  etc.)  of  the 
aorta  and  pulmonary  artery. 

In  the  third  place,  I  believe  that  aortic  murmurs  are  some- 
times present  in  the  early  stages  of  chlorosis,  possibly  they 
would  be  more  frequently  audible  in  such  conditions,  if  it 
were  not  for  the  fact,  that  they  are  so  soft  and  faint  as  to  be 
obscured  at  the  base  by  the  pulmonary  murmur,  and  of  such 
low  tension,  and  of  such  little  force,  as  to  be  inaudible  over  the 
course  of  the  aorta  and  in  the  carotids. 

(2.)  Because  the  point  of  maximum  intensity  of  the  mur- 
mur •  is  not  over  the  pulmonary  artery  at  all,  but  from  one  to 
two  inches  to  the  left  of  the  sternum,  in  the  second  interspace.'^ 

This  argument  also  fails  to  convince  me,  for  the  reasons 
already  detailed.     (See  p.  190.) 

(3.)  Because  no  murmur  of  strictly  pulmonary  origin 
could  possibly  be  referred  to  all  four  orifices  in  turn,  as  has 
been  the  case  with  the  haemic  murmur ;  and  second,  because 
however  singular  a  murmur  of  mitral  regurgitation  in  this 
position  may  seem  to  be,  its  causation  is  by  no  means  difficult 
to  understand.'^ 

Neither  of  these  reasons  seems  to  me  to  exclude  the 
pulmonary  hypothesis.      The   mitral  origin   of   the   murmur, 

'  Edinburgh  Medical  Journal^  Oct.  1S82,  p.  295.     -  Ibid.  p.  294. 
'  Diseases  of  the  Heart.,  second  edition,  p.  173. 


Functional  Miiruiurs.  207 

which  Dr  Balfour  supports,  would  be  as  efifectually  excluded 
by  the  first  reason,  as  he  argues  the  pulmonary  origin  is  ; 
for  no  murmur  of  strictly  mitral  origin  could  possibly  be 
referred  to  all  four  orifices  in  turn.  The  only  legitimate 
conclusion  to  be  drawn  from  the  first  reason  is,  that  in  chlo- 
rosis, murmurs  may  be  generated  at  more  than  one  orifice,  a 
conclusion  which  we  all  allow.  The  second  reason,  even  if 
admitted,  docs  not  exclude  the  pulmonary  hypothesis,  but 
only  shows  that  a  mitral  murmur  can  be  heard  in  the  neigh- 
bourhood of  the  pulmonary  artery. 

I  feel  compelled,  therefore,  to  differ  from  Dr  Balfour ; 
for  I  do  not  see  that  any  argument  which  has  been  as 
yet  advanced  conclusively  negatives  the  purely  pulmonary 
theory. 

As  I  have  previously  stated,  the  sudden  propulsion  of  a 
large  blood-wave,  of  abnormal  (spanaemic)  composition  into 
the  vessel,  which  is  possibly  dilated,  seems  to  me  an  efficient 
cause  for  the  production  of  the  murmur ;  and  we  know,  as  a 
matter  of  fact,  that  in  cases  of  chlorosis  these  conditions  are 
actually  present— the  chlorotic  heart  is  unusually  irritable  and 
contracts  with  unusual  suddenness  ;  even  in  the  earlier  stages, 
there  is  some  dilatation  of  the  right  ventricle  ;  the  blood  is 
spanaemic,  and  in  some  advanced  cases,  i.e.  fatal  cases  of 
pernicious  ansemia,  the  pulmonary  artery  is  dilated. 

Dr  Balfour  himself  states,  in  the  passage  I  have  quoted 
above,  that  aortic  and  pulmonary  murmurs  do  occur  in  the 
later  stages  of  chlorosis,  and  that  the  active  cause  in  .the 
production  of  both  is  the  large  blood-wave  sent  on  by  the 
dilated  and  hypertrophied  ventricles.  Now,  if  aortic  and  pul- 
monary murmurs  can  be  produced  by  this  cause  in  the  later 
stages  of  chlorosis,  and  after,  as  Dr  Balfour  argues,  tricuspid 
and  mitral  regurgitation  have  occurred ;  should  they  not  a 
fortiori  be  produced  in  the  earlier  stages,  before,  as  I  main- 
tain, there  is  sufficient  evidence  of  mitral  and  tricuspid  regurgi- 
tation, for  would  not  the  presence  of  a  leak  at  the  tricuspid 
and  mitral  orifices  diminish  the  size  of  the  blood-wave,  and 
so,  other  things  being  equal,  be  likely  to  interfere  with  the 
production  of,  rather  than  to  cause  such  murmurs  ? 


2o8  Diseases  of  the  Heart. 

The  Differential  Diagnosis  of  Cardiac  Mnnmirs. 
Given  the  presence  of  a  murmur  over  the  praecordia,  we 
have  to  determine  : — 

1.  Whether  it  is  exocardial  or  endocardial. 

2.  If  exocardial,  whether  it  is  a  pleural,  a  pericardial, 
or  a  pericardial-pleural  murmur. 

If  endocardial : — 

3.  The  valve  at  which  it  is  produced,  and  whether  it  is 
direct  or  regurgitant. 

4.  Whether  it  is  organic  or  functional. 

5.  If  organic,  the  extent  and  gravity  of  the  lesion. 
Many  of  these  points  I  shall  afterwards  have  to  consider 

in  detail,  in  treating  of  the  diagnosis  and  prognosis  of  the 
individual  cardiac  affections,  but  it  may  perhaps  be  well, 
even  at  the  risk  of  some  future  repetition,  to  consider  the 
subject  now  as  a  whole,  and  to  point  out  the  leading  facts 
and  circumstances  which  enable  us  to  form  an  opinion  on 
these  important  questions. 

Step  No.  I.     Differential  Diagnosis  of  Exocardial  and 
Endocardial  Miinniirs. 

This  question  is,  as  a  rule,  easily  determined  b}'  attention 
to  the  following  points  :  — 

I.  The  Rhythm  of  the  Mnrninr. — Pleural  friction  sounds  are 
of  course  at  once  distinguished  (except  in  the  case  of  the  peri- 
cardial-pleural friction  murmur,  which  I  shall  presently  refer 
to)  from  cardiac  murmurs  by  the  fact,  that  they  correspond 
in  rhythm  or  frequency  to  inspiration  and  expiration,  and 
that  they  do  not  correspond  to  the  pulsations  of  the  heart. 

Exocardial  murmurs  (pericardial  and  pericardial-pleural 
friction  murmurs)  correspond  in  rhythm  or  frequency  to 
the  pulsations  of  the  heart,  but  their  synchronism  is,  as  a 
rule,  much  less  perfect,  i.e.  they  do  not  correspond  so  exactly 
to  the  heart  sounds,  as  do  endo-cardial  murmurs. 

Pericardial  murmurs,  when  typical,  are  double  (to-and-fro 
friction  sounds),  but  the  murmur  of  combined  aortic  stenosis 
and  incompetence  is  also  double  ;  hence  in  the  majority  of 
cases  the  problem  resolves  itself  into  the  differential  diag- 
nosis of  these  two  conditions,  viz.,    pericarditis   and   double 


Diffei'ential  diagnosis  of  Cardiac  Miirvmrs.   209 

aortic  disease — a  point  which  will  afterwards  be  considered 
in  detail. 

The  rhythm  of  exocardial  murmurs  is,  as  a  rule,  more 
variable  than  the  rhythm  of  endocardial  murmurs.  The 
character  and  the  rhythm  of  the  murmur  is  apt  to  change 
from  day  to  day,  from  hour  to  hour,  or  even  during  the  actual 
examination  of  the  patient,  a  fact  which  is  explained  by  the 
circumstance  that  the  relative  positions  of  the  two  opposed 
and  roughened  surfaces  of  the  pericardium  may  be  materially 
modified  by  alterations  in  the  position  of  the  patient,  and 
the  pressure  of  the  stethoscope.^  The  fact  that  alterations 
in  tone  and  rhythm  can  be  produced  by  the  pressure  of  the 
stethoscope  is  highly  characteristic  of  pericardial  murmurs. 

2.  Tlie  sound  characters  of  the  murmur.  —  Exocardial 
murmurs  are  friction  sounds,  and,  as  a  rule,  have  a  harsh, 
grating  character  ;  they  usually  appear  to  be  superficial.  But 
this  and  their  other  characters  I  have  previously  described. 
(See  p.  167.) 

3.  The  point  of  maximum  intensity  of  tJic  murmur,  and 
tlie  direction  in  w/iich  it  is  propagated. — Exocardial  murmurs 
are,  as  a  rule,  best  heard  over  the  centre  of  the  right 
ventricle  or  at  the  base  of  the  heart  ;  but  they  have  no 
special  points  of  differential  maximum  intensity  as  endo- 
cardial murmurs  have.  Exocardial  murmurs  are  often  only 
heard  over  a  very  limited  area,  and  they  are  not  propagated 
in  any  definite  direction  as  endocardial  murmurs  are. 
(See  p.  182.) 

4.  The  associated  symptoms  and  Jiistory  of  the  case.  —  Exo- 
cardial murmurs  appear  abruptly,  so  to  speak,  and  generally 
in  the  course  of  some  constitutional  affection  such  as  rheu- 
matic fever,  Bright's  disease,  etc.  Endocardial  murmurs 
may  appear  abruptly  and   in  the  course  of  rheumatic  fever, 

'  Endocardial  murmurs  are  sometimes  only  audible  in  one  particular  position. 
The  presystolic  murmurs,  for  example,  may  disappear  when  the  patient  sits  up,  as 
Professor  Sydney  Ringer  and  others  have  noted.  Again,  other  endocardial  mur- 
murs are  very  decidedly  intensified  by  sitting  up,  walking,  etc.  But  in  these  cases 
the  rhythm  of  the  murmur  remains  the  same,  and  is  not  modified  by  alterations  i'n 
position. 

O 


2IO  Diseases  of  the  Heart. 

but,  in  many  cases,  the  lesion  which  produces  them  develops 
very  slowly.  The  absence  of  constitutional  disturbance,  and, 
especially,  the  fact  (if  such  a  history  can  be  obtained)  that 
the  murmur  is  an  old  one,  are  strongly  in  favour  of  its  endo- 
cardial origin. 

Step  No.  2.      The  Munnur  is  Exocardinl ;  is  it  a  Pleural, 
Perieardial,  or  Pericardial-pleural  Aluruiur  ? 
Ordinary  pleural  friction  is  at  once  distinguished  by  the 
fact,  that  its  rhythm  corresponds  to  the  rhythm  of  the  respi- 
ratory movements. 

Pericardial-pleural  friction  is  extremely  rare.  It  occurs, 
as  I  have  previously  explained,  when  that  portion  of  the 
pleura,  which  is  reflected  over  the  pericardium  is  inflamed  ; 
and  it  is  produced  by  the  movements  of  the  heart  rubbing 
this  rough  and  inflamed  portion  of  the  pleura  against  the 
anterior  wall  of  the  chest,  or  against  the  visceral  pleura  which 
is  in  contact  with  it.  The  points  by  which  we  are  enabled  to 
distinguish  pericardial-pleural  friction  from  ordinary  pleural 
friction  are  as  follows  — 

1.  Pericardial-pleural  friction  is  generally  best  heard  over 
the  borders  of  the  heart,  i.e.  where  the  visceral  and  parietal 
portions  of  the  pleura  come  into  contact  ;  whereas  ordinary 
pericardial  friction  is,  as  a  rule,  best  heard  over  the  centre  of 
the  cardiac  dulness,  i.e.  over  the  centre  of  the  anterior  surface 
of  the  right  ventricle. 

2.  Pericardial-pleural  friction  is,  as  a  rule,  more  afl"ected 
by  the  respiratory  movements  than  ordinary  pericardial  fric- 
tion. I  have,  in  two  cases,  observed  that  it  was  decidedly 
increased  by  a  full  inspiration,  i.e.  when  a  larger  portion  of 
the  two  inflamed  surfaces  of  the  pleura  were  brought  in  con- 
tact. Walshe  states  that  it  is,  as  a  rule,  increased  during 
expiration  ;  and  in  such  cases  the  murmur  is  probably  pro- 
duced by  friction  between  the  outside  of  the  pericardium  and 
the  inside  of  the  chest  wall.  When  the  patient  takes  a  deep 
inspiration,  the  pericardial-pleural  friction  is  sometimes  re- 
placed by  ordinary  pleural  friction.  This  is  not  pathogno- 
monic, for  pericarditis  is  not  unfrequently  accompanied  by 
pleurisy,  and,  in  such  cases,  the  pericardial  friction  may  only 


Differential  diagnosis  of  Cardiac  Murmurs.   2 1 1 

be  observed  over  the  praecordial  region  during  a  deep 
inspiration,  and  may  then  replace  the  pericardial  friction 
sound. 

3.  In  pericardial-pleural  friction  we  should  expect  to  find 
the  symptoms  of  pleurisy,  but  there  would  be  no  indications 
of  pericarditis  ;  and  vice  versa.  It  must  not,  however,  be 
forgotten  that  many  cases  of  dry  pericarditis  are  unattended 
by  any  symptoms  or  signs  except  the  to-and-fro  friction 
murmur. 

4.  The  pericardial-pleural  friction  murmur  is  even  more 
variable  than  the  ordinary  pericardial  friction  murmur ;  and 
may  even  cease  with  certain  pulsations  of  the  heart. 

Step  No.  J. —  The  IMuruiur  is  Ejidocardial ;  at  zuhich  valve 
is  it  produced,  and  is  it  direct  or  regurgitant  f 
The  valve  at  which  the  murmur  is  produced  is  determined 
by  observing  : — 

1.  The  point  of  differential  maximum  intensity  of  the 
murmur.     (See  page  180.) 

2.  The  direction  in  which  it  is  propagated.  (See  page  182.) 

3.  The  effect  which  the  lesion  has  produced  upon  the 
heart  and  circulation.  It  will  be  more  convenient  to  con- 
sider this  point  when  speaking  of  the  character  of  the  lesion. 
(See  page  214.) 

4.  The  relative  frequency  of  the  different  valvular  lesions. 
This  is  not  a  point  of  very  much  importance,  for  it  is  gene- 
rally easy  to  decide  the  question  by  the  points  already  men- 
tioned (1,2,  and  3)  ;  but  in  some  doubtful  cases,  as,  for  in- 
stance, in  the  case  of  a  murmur  heard  over  the  base  of  the 
heart,  the  fact  that  the  pulmonary  orifice  is  very  rarely  dis- 
eased after  birth,  would,  supposing  that  we  could  exclude 
inorganic  conditions,  be  strongly  in  favour  of  the  aortic  origin 
of  the  murmur. 

The  question  whether  the  murmur  is  direct  or  regurgitant 
is,  of  course,  easily  decided,  by  observing  its  rhythm.  (See  page 
172.)  When  it  is  difficult  or  impossible  to  determine  the 
rhythm,  the  sound  characters  of  the  murmur,  and  the  effects 
of  the  lesion  on  the  heart  and  circulation  are  the  points  which 
must  be  chiefly  relied  upon. 


2  I  2  Diseases  of  tiie  Heart. 

Step  Xo.  ^. — The  Murmur  is  Endocardial ;  is  it  Organic  or 
Functional  / 
It  is  sometimes  very  difficult,  or  even  impossible,  to  give  a 
positive  answer  to  this  question  ;  in  other  cases  it  is  decided 
with  the  greatest  ease.  The  difficulty  is  greatest  in  the 
case  of  mitral  systolic  murmurs,  which  result  so  frequently 
from  'muscular'  and  'relative'  incompetence,  and  in  which 
therefore  we  have  to  decide  whether  the  muscular  weakness 
of  the  heart  is  curable  or  not.  In  such  cases  it  is  only  by 
taking  a  broad  and  general  view  of  all  the  features  of  the 
case  — independently  of  the  mere  physical  examination  of  the 
heart  itself — that  a  correct  conclusion  can  be  arrived  at. 

In  practice,  the  first  step  in  the  differential  diagnosis  of 
organic  and  functional  murmurs  is  to  determine  the  rhythm  of 
the  murmur.  The  so-called  functional  murmurs  are,  as  we 
have  already  seen,  always  systolic,  and  may  be  heard  either 
in  the  pulmonary,  aortic,  mitral,  or  tricuspid  areas.  If,  then, 
the  murmur  is  diastolic  or  presystolic,  we  may  with  certainty 
conclude  that  it  is  organic.  (As  I  have  previously  stated. 
Professor  Austin  Flint  believes  that  a  mitral  lesion  is  not 
essential  for  the  production  of  a  presystolic  murmur.  The 
matter  is  perhaps  of  less  practical  moment  than  would  at 
first  sight  appear.  For  since  Professor  Flint  only  claims  to 
have  noted  this  presystolic  murmur,  without  mitral  lesion,  in 
cases  of  aortic  incompetence  ;  and  since  aortic  incompetence 
is  always  an  organic  and  serious  lesion,  the  matter  is,  so  far 
as  our  present  purpose  is  concerned,  comparatively  unim- 
portant, i.e.  so  far  as  concerns  the  decision  whether  the  cardiac 
lesion  is  temporary  and  curable,  or  organic  and  incurable.) 

If  the  rhythm  of  the  murmur  does  not  decide  the  ques- 
tion— that  is  to  say,  if  the  murmur  is  systolic — we  must 
seek  to  determine  the  question  by  attention  to  the  following 
points  : — 

(a.)    Tin    presence    or   absence   of   the    causes    of  inorganic 

murmurs  on  the  one  liand,  or  of  organic  murmurs  on  the  other. 

The  structural  changes  of  a  temporary'  kind  which  affect 

the  heart  muscle  in  ansemia  and   the   continued   fevers,  are 

the   great    causes    of  the    so-called    inorganic    or    functional 


Differential  diagJiosis  of  Cardiac  Aliiruiurs.     2  1 3 

murmurs.  A  murmur,  then,  occurring  in  a  patient,  who  is 
neither  anremic  nor  suffering  from  one  of  the  continued 
fev^ers,  is  probably  organic.  The  reverse  proposition  (that 
murmurs,  occurrmg  in  persons  who  are  anaemic  or  suffering 
from  one  of  the  continued  fevers,  are  functional)  does  not 
necessarily  hold  good.  This  caution  more  particularly  applies 
to  cases  of  rheumatic  fever  in  which  there  is  a  strong  ten- 
dency to  inflammatory  affections  of  the  heart,  but  in  which 
functional  murmurs  due  to  anaemia  and  to  temporary  and 
curable  alterations  in  the  heart  muscle,  are  also  frequently 
developed.  Murmurs,  then,  which  develop  in  the  course  of 
rheumatic  fever,  are  probably,  but  not  necessarily,  organic. 
It  is  unnecessary  to  detail  here  the  ordinary  symptoms  of 
anaemia;  the  pallor  of  the  mucous  membranes,  and  the  pre- 
sence of  a  venous  hum  in  the  neck,  are  the  points  of  most 
importance. 

(b.)  'J  fie  condition  of  tlie  Iieart  and  circulation.  This  some- 
times gives  us  important  information,  as  in  the  following 
case : — 

Case. — J.  B.,  aet.  51,  was  admitted  to  the  Ne\vcastIe-on-Tyne  Infirmary 
under  my  care  on  29th  November  1878,  complaining  of  shortness  of 
breath  and  of  swelling  of  the  feet.  He  was  very  ansmic  ;  a  well-marked 
systolic  murmur  was  audible  over  the  aortic  area  ;  the  left  ventricle  was 
not  markedly  hypertrophied.  The  pulse  was  slow  and  deliberate,  and 
the  apex  of  the  sphygTiiographic  tracing  rounded.  These  characters 
which  are  seen  in  figure  55,  seemed  to  show  that  the  aortic  murmur  was 
not  merely  haemic,  but  that  it  was  due  to  organic  stenosis  of  the  aortic 
orifice. 


Fig.  55. — Sphygmogram  from  the  case  of  |.  B.,  referred  to  in  the  text. 

It  must,  however,  be  remembered,  that  free  mitral 
regurgitation  may  be  due  to  temporary  and  curable  con- 
ditions ;  and  that  in  such  cases  all  the  symptoms  and  signs 
of  regurgitation  due  to  organic  and  incurable  disease  (viz., 
accentuation    of   the    pulmonary    second   sound,  changes    in 


2  14  Diseases  of  the  Heart. 

the  right  heart,   shortness  of  breath,   dropsy,   etc.),  may  be 
present. 

(c.)  The  effect  of  treatment. — This  is  a  most  valuable,  and 
indeed,  in  some  cases,  the  only  certain  means  of  deciding 
whether  a  murmur  is  functional  or  organic. 

(d.)  The  point  of  inaximnm  intensity  of  the  imirnmr  and 
the  extent  of  its  propagation. — These  points  may  also  give  us 
some  information.  Anaemic  murmurs  are  generally  basic,  and 
are  most  commonly  heard  over  the  pulmonary  area,  often  also 
over  the  aorta,  more  rarely  at  the  apex.  Inorganic  murmurs 
are  not  so  well  propagated  as  organic  ones  ;  aortic  murmurs, 
therefore,  which  are  carried  into  the  vessels  of  the  neck,  and 
mitral  murmurs,  which  are  audible  at  the  inferior  angle  of  the 
left  scapula,  are  probably  organic. 

{e.)  The  history  of  the  case. — This  may  be  of  importance  ; 
a  history  of  rheumatic  fever  would,  other  things  being  equal 
{i.e.  in  a  doubtful  case),  be  strongly  in  favour  of  the  organic 
nature  of  the  case. 

The  differential  diagnosis  of  functional  and  organic 
murmurs  will  be  considered  in  further  detail  when  the 
individual  valvular  lesions  are  treated  of.     (See  chapter  V.) 

Step  No.  J. —  The  Mnrimir  is  Organic  ;  zvhat  is  the  extent  and 
gravity  of  the  Lesion  ? 

The  extent  of  the  lesion.— 0\.\\qx  things  being  equal,  the 
more  extensive  the  lesion,  the  more  serious  the  case.  Now, 
in  recent  cases  it  may  be  very  difficult,  or  even  impossible 
to  determine  the  exact  extent  of  the  lesion.  It  may  be 
impossible,  for  instance,  to  say  what  proportion  of  the  symp- 
toms, is  due  to  temporary  conditions,  and  how  far  the  morbid 
conditions  may  be  restored  or  compensated. 

In  chronic  cases  the  extent  of  the  lesion  is  more  easily 
determined,  and  in  order  to  arrive  at  a  correct  conclusion  the 
following  circumstances  must  be  taken  into  account : — 

I.  TJie  effect  of  the  lesion  upon  the  heart  and  the  circulation. 
— As  we  shall  afterwards  see,  the  great  effect  of  all  valvular 
lesions  is  to  prevent  the  steady  onward  passage  of  the  blood 
current.     In  seeking,   therefore,  to   estimate  the  extent  and 


Diffei'entiai  diagnosis  of  Cardiac  Murmurs.    2  1 5 

gravity  of  any  valvular  lesion,  it  is  necessary  to  examine  the 
effects  produced: — {A.)  In  the  cavities  of  the  heart,  and  in 
the  parts  of  the  circulation  which  are  situated  behind  the 
lesion  —  the  backivard  effects;  {B.)  In  the  cavities  of  the 
heart  and  parts  of  the  circulation  which  are  situated  in  front 
of  the  lesion  —  the  forward  effects^  as  they  may  be  termed. 
The  more  marked  these  effects,  and  the  shorter  the  period 
which  has  been  required  for  their  full  development,  in  other 
words,  the  more  rapid  the  progress  of  the  case,  the  worse  the 
prognosis.  It  will  be  necessary,  therefore,  in  the  next  place, 
to  consider  the  effects  which  the  different  valvular  lesions 
tend  to  produce  on  the  circulation  in  front  and  behind,  and 
the  symptoms  which  result  therefrom.  I  say,  tend  to 
produce,  for  it  is  essential  to  remember  that  serious  valvular 
lesions  may,  for  a  time  at  least,  be  unattended  by  any 
apparent  external  effects  or  symptoms — a  point  which  I  have 
already  insisted  upon  in  speaking  of  the  important  '  principle 
of  compensation.'  On  the  other  hand  it  is  no  less  important 
to  remember,  that  in  these  cases  {i.e.  in  cases  of  serious 
valvular  lesions,  which  are  so  perfectly  compensated,  as  to  be 
unattended  by  any  apparent  external  effects  or  symptoms  so 
long  as  the  circulation  is  not,  so  to  speak,  put  upon  the 
stretch)  there  are  internal  effects  (such  as  hypertrophy  of  the 
heart,  etc.)  which  can  be  detected  by  physical  examination. 

The  effects  which  the  different  valvular  lesions  tend  to 
produce  on  the  heart  and  circulation  are  as  follows  : — 

MITRAL   STENOSIS. 

A.  Backward  Effects.  (a)  Blood  stagnates  in  the  left 
auricle,  which  becomes  over-distended,  hypertrophied,  and 
dilated  ;  {b)  The  pulmonary  veins  become  engorged  ;  {c)  The 
lungs  become  congested  :  lung  symptoms,  consisting  of  short- 
ness of  breath,  especially  on  exertion,  going  up  stairs  or  up 
a  hill  ;  a  tendency  to  catarrhal  affections  of  the  lungs  and 
bronchi  (especially  chronic  bronchitis),  to  oedema  of  the  lungs, 
to  haemoptysis,  to  hydrothorax,  etc.,  are  apt  to  arise  ;  id)  The 
increased  blood-pressure  in  the  pulmonary  artery  produces 
accentuation  of  the  pulmonary  second  sound  ;  and  there  is, 


2i6  Diseases  of  the  Heart. 

in  many  cases,  reduplication  of  the  second  sound  of  the  heart  ; 
{e)  The  right  ventricle  becomes  hypertrophied  and  dilated  ; 
(/J  Tricuspid  regurgitation  not  unfrequently  occurs  with  pul- 
sation in  the  veins  of  the  neck.^  (The  enlargement  of  the 
right  cavities  of  the  heart,  both  ventricle  and  auricle,  and  the 
presence  of  tricuspid  regurgitation,  can  be  ascertained  by 
physical  examination)  ;  {g)  The  systemic  venous  circulation 
is  impeded,  and  the  symptoms  which  result  from  this  venous 
engorgement  are  often  the  first  which  attract  the  attention  of 
the  patient.-  The  peripheral  parts,  more  especially  the  lips, 
nose,  and  ears,  tend  to  become  cyanotic,  and  the  face  some- 
what full  and  swollen.  Dropsy,  commencing  in  the  feet 
(increased  by  standing  and  walking,  and  therefore  worse  at 
night),  gradually  extends  upwards,  and  finally  involves  the 
serous  cavities  as  well  as  the  subcutaneous  tissues  of  the 
lower  parts  of  the  body.  Engorgement  of  the  portal  vessels 
produces  congestion  of  the  liver,  stomach,  and  haemorrhoidal 
veins,  with  resulting  enlargement  of  the  liver,  muddiness  of 
the  complexion  or  slight  jaundice,  dyspepsia,  and  piles. 
Congestion  of  the  renal  veins  is  attended  with  scanty  and 
high  coloured  urine,  which  is  loaded  with  urates,  and  often 
contains  albumen.  Interference  with  the  return  current  from 
the  brain  may  be  attended  with  drowsiness  and  other  indica- 
tions of  mental  obfuscation. 

B.  Forward  Effects. —  Small  and  variable  quantities  of 
blood  are  passed  into  the  left  ventricle  through  the  stenosed 
orifice  ;  consequently  small  and  variable  quantities  of  blood 
are  pumped  into  the  arterial  system,  the  pulse  being,  there- 
fore, small,  unequal  in  volume,  and  irregular  in  time.  (So 
long  as  the  compensation  is  well  maintained,  the  volume 
and  rhythm  of  the  pulse  ma}'  not  be  much  altered.)  The 
occurrence  of  a  second  and    imperfect  ventricular  contraction 


'  For  the  reasons  previously  given,  the  accentuation  of  the  puhnonary  second 
sound  may  diminish  or  disappear  with  the  occurrence  of  tricuspid  regurgitation. 

*  In  this  description  I  have  sketched  the  backward  effects  in  their  anatomical, 
rather  than  their  chronological  sequence,  venous  engorgement  and  its  resulting 
s)TTiptoms  occurring  long  before  many  of  the  other  conditions,  such  as  tricuspid 
regurgitation. 


Differential  diagnosis  of  Cardiac  Mnrmurs.     2  i  7 

in  the  sphygmographic  tracing,  such  as  is  shown   in  fig.   56, 
is  often  obscr\-ed. 


Pressure  3'^  oz. 

Fig.  56. — Irregularity  of  the  Pulse. — W.  M.,  ajt.  50,  admitted  to  Newcastle 
Infirmary  30th  November  1878,  suffering  from  the  usual  symptoms  of 
mitral  disease.  The  heart's  action  was  extremely  irregular  The  left 
ventricle  much  hypertrophied.  There  was  no  rheumatic  history.  The 
symptoms  were  of  two  months'  duration. 

I  have  attempted  in  figs.  57,  58  to  represent  in  a  diagram- 
matic manner,  the  backward  effects  which  mitral  lesions 
produce  on  the  heart  and  circulation. 


A 

\ 

^'—:/j0^ 

^^S 

■'^^y 

"] 

^ 

V 

V'--; 

\ 

--A' 

,# 

^Ssj 

^-„L 

n 

Y— 

i   :',— - 

PA-^# 

--..,- 

^^ 

-C-PV 

'- 

-A 

R4— 

.'    »^ 

1    ^   -j— -RV 

Li\.-{ 

V 

^) 

— LV 

Fig.  57. — Representation  of  the  effects  of  a  lesion  of  the  mitral  valve  (mitral 
stenosis  in  this  case)  on  the  heart  and  circulation.  The  effects  of  mitral 
regurgitation  are  the  same,  but  there  is,  in  addition,  hypertrophy  of  the 
left  ventricle.  LV=left  ventricle;  L.-\.  =  left  auricle;  PV=pulmonary 
veins;  L  =  lungs ;  PA=puImonary  artery;  RV  =  right  ventricle;  RA= 
right  auricle;  V  =  venK  cavas ;  V'=venous  system;  B'  =  termination  of 
the  venous  system  in  the  systemic  capillaries;  A  =  the  aorta;  A'=the 
arterial  system.  The  arrows  show  the  direction  of  the  backward  pressure. 
The  dotted  lines  show  the  effects  of  the  obstruction  (dilatation)  on  the 
different  parts. 


2l8 


Diseases  of  the  Heart. 


Fig.  58. 


Differential  diagjiosis  of  Cardiac  Murmurs.     219 

MITRAL   REGURGITATION. 

A.  Backward  Effects. — The  backward  effects  are  similar 
to  those  which  are  produced  by  mitral  stenosis.  As  a  rule 
grave  disturbances  of  the  circulation  are  manifested  earlier  in 
mitral  regurgitation  than  in  stenosis — a  fact  which  is  easily 
understood  when  we  remember  that  in  many  cases  the  former 
results  from  degeneration  and  failure  of  the  heart  muscle, 
independently  of  any  lesion  of  the  valvular  segments. 

B.  Forivard  Effects. — The  pulse  is  small,  and  in  advanced 
cases  (i.e.  after  the  failure  of  compensation),  it  is  usually 
irregular. 

AORTIC   STENOSIS. 

A.  Backivard  Effects. — The  left  ventricle  becomes  hyper- 
trophied  in  consequence  of  the  increased  effort  required  to 
force  the  blood  through  the  stenosed  orifice  ;  but  so  long  as 
the  mitral  valve  remains  competent — and  it  usually  does  so 
even  in  advanced  cases — there  are  no  prominent  lung 
symptoms,  or  other  signs  of  venous  engorgement. 

B.  Forzuard  Effects.  —  The  pulse  is  small  but  of  good 
tension,  slow  and  regular.  When  the  stenosis  is  considerable, 
symptoms  due  to  defective  blood-supply  to  the  brain  are 
sometimes  observed. 

AORTIC    REGURGITATION. 

A.  Backward  Effects. — The  left  ventricle  becomes  hyper- 
trophied  and  dilated,  and  in  consequence  of  the  dilatation 
of  the  cavity  and  the  impaired  nutrition  of  the  cardiac 
muscle,  mitral  regurgitation  is  common  towards  the  later 
stages  of  the  case.  So  long  as  the  mitral  valve  remains 
sound  there  are  no  prominent  lung  symptoms  or  other  signs 
of  venous  engorgement  ;  should  the  mitral  give  way  the 
symptoms  characteristic  of  mitral  regurgitation  are  super- 
added to  the  symptoms  which  I  must  now  describe. 

B.  Forward  Effects. — At  each  systole  of  the  dilated  and 


Description  of  Fig.  j8. 
Diagrammatic  representation  of  the  effects  of  a  mitral  lesion  upon  the  venous  circu- 
lation.    The  numbers  and  letters  are  the  same  as  in  fig  3.    (See  description 
page  5. )     The  arrows  indicate  the  direction  of  the  backward  current. 


220 


Diseases  of  the  //earl. 


hypertrophied  left  ventricle,  a  large  quantity  of  blood  is  pro- 
pelled into  the  arterial  system,  which  is  therefore  rapidly  and 
fully  distended  ;  but,  in  consequence  of  the  leak  at  the  aortic 
orifice,  this  distention  of  the  arterial  system  is  not  maintained. 
The  pulse  is  highly  characteristic,  presenting  the  jerking, 
visible,  collapsing,  water-hammer  character  which  was  so  ably 
described  by  the  late  Sir  Dominic  Corrigan  (Corrigan's  pulse.) 
It  is  generally  quicker  than  in  health.  The  aortic  and  dicrotic 
wave  is,  as  a  rule,  feebly  marked  or  absent,  and  the  sphygmo- 
graphic  tracing  is,  in  some  cases,  characteristic.  When  the 
regurgitation  is  free,  the  artery  may  be  very  empty  during  the 
ventricular  diastole.  The  face  is  generally  pale,  and  usually 
presents  an  anxious  expression.  In  advanced  cases,  attacks 
of  syncope  are  common,  and  the  general  condition  of  nutrition 
may  be  considerably  impaired.  Pain  of  an  angina-like  char- 
acter is  frequently  observed.  The  amount  of  alteration  in  the 
pulse,  more  especially  the  degree  of  distention  during  the 
ventricular  diastole  ;  the  extent  of  the  dilatation  of  the  left 
ventricle  ;  and  the  condition  of  the  mitral  valve — whether 
competent  or  not — are  points  of  great  importance  in  estimating 
the  gravity  of  this  lesion. 

Figure  59  represents  in  a  diagrammatic  manner  the  effects 
of  aortic  lesions  upon  the  circulation. 


^H 

^^^^H 

^B^^^^^^ 

■H 

■^^^^^^Sv 

Bll 

■S^^^^^ba 

^^W 

Bll 

KiG.  59. — Representation  of  the  effects  of  a  lesion  of  the  aortic  valves  (aortic 
regurgitation  in  this  case)  on  the  heart  and  circulation.  The  letters  have 
the  same  significance  as  in  fig.  57.  The  left  ventricle  is  hypertrophied 
and  dilated  ;  the  mitral  valve  is  as  yet  competent. 


Differential  diagnosis  of  Cardiac  Munnnrs.      221 

PULMONARY   AND   TRICUSPID  LESIONS. 

The  effects  produced  by  pulmonary  and  tricuspid  lesions 
will  be  readily  understood  after  what  has  been  already  stated 
in  describing  the  effects  of  mitral  lesions. 

Pulmonary  lesions — which  are  extremely  rare,  except  as 
congenital  conditions — produce  alterations  in  the  right  cavities 
of  the  heart  and  engorgement  of  the  systemic  venouscirculation. 

Tricuspid  regurgitation  (which  is  frequent  in  the  advanced 
stages  of  mitral  lesions,  and  which  may  also  arise,  as  I  have 
previously  pointed  out,  from  primary  disease  of  the  lungs, 
such  as  emphysema  and  cirrhosis)  is  always  attended  with 
marked  signs  of  systemic  venous  engorgement.  Venous 
pulsation  in  the  neck,  synchronous  with  the  contraction  of 
the  right  ventricle,  is  very  characteristic  of  this  condition  ; 
and  in  some  cases  true  pulsation  in  the  liver,  the  result  of  a 
back-wash  through  the  inferior  cava,  is  observed. 

2.  TJie  ainoiint  of  compensation  ivhch  can  be  produced.  —  In 
all  valvular  lesions  there  is  an  attempt  on  the  part  of  nature 
to  meet  the  difficulty.  The  extent  to  which  the  lesion  can 
be  compensated,  and  the  probable  time  during  which  this 
compensation  can  be  maintained,  are  most  important  points 
in  estimating  the  gravity  of  the  lesion.  The  capability  of 
compensation  depends  upon  : — 

{a)  Tlie  general  reparative  pozvers  of  the  individual. — A 
valvular  lesion  of  moderate  extent,  occurring  in  an  individual 
whose  tissues  are  prone  to  degenerate,  or  already  in  a  state 
of  decay,  is  of  graver  significance  than  a  much  more  exten- 
sive lesion  in  a  person  whose  tissues  are  otherwise  healthy. 

if)  The  special  reparative  poiver  of  the  cardiac  uniscle. — So 
long  as  the  cardiac  muscle  remains  sound,  and  the  hyper- 
trophy is  good,  compensation  is  well  maintained,  and  the 
symptoms  are  at  a  minimum.  But  whene\-er  the  muscular 
nutrition  fails,  or  dilatation  occurs,  the  compensation  gradu- 
ally fails,  and  serious  symptoms  arise.  The  structural  sound- 
ness therefore  of  the  cardiac  muscle,  and  the  presence  or 
absence  of  dilatation  are  points  of  great  importance  in 
estimating  the  gravity  of  the  lesion. 


22  2  Diseases  of  the  Heart. 

(c)  The  age  of  the  patient. — Other  things  being  equal,  the 
younger  the  patient,  the  better  the  prognosis,  for  in  young 
persons  the  reparative  powers,  and  therefore  the  capabiHties 
of  compensation,  are  greater  than  in  old  people. 

{d)  The  Jiabits  and  surroundings  of  the  patient. — Valvular 
lesions  are  (other  things,  such  as  the  condition  of  the  tissues, 
being  equal)  much  less  serious  in  persons  in  comfortable 
circumstances  than  in  those  who  are  obliged  to  struggle  for 
existence,  and  lead  laborious  lives.  Indeed,  as  we  shall  see 
when  I  come  to  speak  of  the  treatment  of  these  affections, 
rest — so  far  as  is  possible — to  the  damaged  organ  is  the  first 
and  most  important  point  to  be  attended  to.  The  amount 
of  work  required  of  the  damaged  heart,  is  a  very  important 
element  in  the  prognosis. 

{e)  The  mental  temperament  of  the  patient  is  of  consider- 
able importance.  Valvular  lesions  are  less  serious  in  persons 
of  a  quiet  and  placid  disposition  than  in  persons  of  an 
excitable  and  anxious  temperament. 

(/)  The  cEtiology  of  the  lesion. — Valvular  lesions  of  rheu- 
matic origin  are,  as  a  rule,  less  serious  than  those  which  result 
from  other  causes.  This  is  probably  owing  to  the  facts,  that 
non-rheumatic  valvular  lesions  are  often  due  to  degenerative 
processes,  and  that  persons  thus  affected  are,  as  a  rule,  older 
than  those  affected  with  lesions  which  can  be  directly  traced 
to  acute  rheumatism. 

3.  The  form  of  valvular  lesion. — We  know,  as  the  result 
of  clinical  experience,  that  some  valvular  lesions  are  more 
serious  than  others.  Dr  Walshe  gives  the  following  as  the 
order  of  relative  gravity,  estimating  the  gravity  not  only  by 
the  ultimate  lethal  tendency  of  the  different  lesions,  but  also 
by  the  amount  of  complicated  miseries  which  they  inflict. 
(This  order  can  onl)-  be  looked  upon  as  approximate.  I 
shall  afterwards  have  to  point  out  many  modifications  in 
it.  There  are,  for  instance,  many  different  causes  of  mitral 
regurgitation,  some  of  which  are  eminently  curable  ;  others 
almost  certainly  fatal.  Dr  Walshe  evidently  alludes  to  the 
more  serious  forms.  So  again,  tricuspid  regurgitation  may 
be    a    temporary    and    curable    condition,    though    in     many 


Diffei'cntial  diagjiosis  of  Cardiac  M2i7'miirs.      223 

cases    it    is    the  most   unfavourable    of  all    cardiac  valvular 
lesions): — 

1.  Tricuspid  regurgitation  (most  grave). 

2.  Mitral  regurgitation. 

3.  Mitral  constriction. 

4.  Aortic  regurgitation. 

5.  Pulmonary  constriction. 

6.  Aortic  constriction  (least  grave). 

The  relative  gravity  as  regards  their  tendency  to  produce 
sudden  and  instantaneous  death  is,  however,  quite  different. 
Aortic  regurgitation  stands  prominently  out  as  the  valvular 
lesion  which  often  gives  rise  to  immediate  death,  the  fatal 
result  being  due  to  syncope ;  while  the  other  valvular  lesions 
have  no  direct  tendency  to  produce  immediate  death. 

4.  Whether  the  lesion  is  progressive  or  stationary. — This  is 
an  extremely  important  point,  and  it  is  to  be  determined — 

(a)  By  close  observation  of  the  case,  and  noting  the  condi- 
tion of  the  patient  from  time  to  time. 

{b)  By  comparing  the  duration  of  the  case  and  the  effects 
which  the  lesion  has  already  produced  on  the  heart  and 
circulation. 

{c)  By  taking  into  account  the  nature  of  the  morbid 
process.  We  know  as  the  result  of  clinical  and  pathological 
observation,  that  valvular  lesions,  due  to  degenerative  pro- 
cesses, are  less  likely  to  remain  stationary  than  those  which 
result  from  simple  inflammation  (endocarditis). 

{d)  By  reference  to  the  valve  which  is  affected,  and  the 
manner  in  which  it  is  affected.  Mitral  regurgitation,  for  ex- 
ample, is  in  many  cases  curable,  but  aortic  regurgitation  is  not. 

5.  The  associated  pathological  conditions. — This  is  a  point 
of  the  very  greatest  importance.  In  all  cases  in  which  the 
tissues  are  prone  to  degenerate,  the  prognosis  is  bad  ;  in  fat, 
flabby  individuals,  a  lesion— other  things  being  equal — 
usually  advances  with  more  rapidity,  and  proves  more 
speedily  fatal  than  in  spare  and  thin  people.  The  presence 
of  kidney  disease,  or  of  any  other  organic  lesion,  adds,  of 
course,  very  materially  to  the  gravity  of  the  case. 

The  points  which  enable  us  to  determine  the  extent  and 


2  24  Diseases  of  the  Heart. 

gravity  of  the  lesion  will  be  considered  in  further  detail  under 
the  prognosis  of  the  individual  valvular  lesions. 

THE   PHYSICAL   EXAMINATION    OF   THE   AORTA   AND  THE 
GREAT    BLOOD   VESSELS. 

After  having  ascertained  the  condition  of  the  heart  itself. 
we  must  next  determine  the  physical  condition  of  the  aorta 
and  great  blood-vessels.  In  actual  practice  it  is  customary 
and  convenient  to  examine  the  condition  of  the  arch  of  the 
aorta,  and  of  the  heart,  at  one  and  the  same  time  ;  when  in- 
specting the  praecordia,  for  example,  to  inspect  at  the  same 
time  the  parts  of  the  chest  which  lie  superficial  to  the  aortic 
arch  ;  and  so  on  with  palpation,  percussion,  and  auscultation. 
In  ordinary  cases  it  is  not  customary  to  make  a  detailed 
examination  of  the  great  branches  of  the  aortic  arch,  or  of  the 
descending  thoracic  or  abdominal  portions  of  the  aorta. 
When,  however,  there  is  any  reason  to  suspect  disease  of  these 
structures,  their  condition  must  be  carefully  and  methodically 
examined. 

In  order  to  ascertain  the  physical  condition  of  the  aorta 
(both  its  thoracic  and  abdominal  portions)  and  of  its  branches, 
we  employ  the  same  means  of  investigation  which  I  have 
already  described  in  speaking  of  the  physical  examination  of 
the  heart : — 

Firstly  we  inspect,  palpate,  percuss,  and  auscultate  the 
parts  superficial  to  the  vessel. 

Secondly,  we  investigate  the  condition  of  the  circulation 
and  of  the  circulatory  organs  in  front  and  behind  ;  when  we 
are  investigating  the  condition  of  the  aortic  arch,  for  instance, 
we  direct  special  attention  on  the  one  hand  to  the  condition 
of  the  pulse  in  the  different  branches  arising  from  it  {i.e.  we 
observe  the  comparative  condition  of  the  pulse  in  the  two 
radials  and  carotid  arteries),  and  on  the  other  to  the  state  of 
the  heart  and  venous  circulation. 

Thirdly,  we  pay  special  attention  to  the  physical  condition 
of  the  organs  and  parts  adjacent  to  the  vessel.  This  is  a 
point  of  great  importance,  for  the  chief  pathological  conditions 
in  the  aorta  and   its  branches,  which  we  are  able  to  ascertain 


The  Exaiuiuation  of  tJic  thoracic  aorta.  225 

by  means  of  physical  examination,  are  dilatations  (simple  and 
aneurismal)  and  the  chief  symptoms  and  physical  signs  in 
these  conditions  are  often  due  to  the  pressure  of  the  dilated 
blood  vessel  upon  adjacent  parts,  and  to  the  displacements 
which  are  caused  thereby. 

INSPECTION  APPLIED  TO  THE  EXAMINATION  OF  THE 
THORACIC  AORTA. 

The  patient  should  be  placed  in  a  good  light,  and  the 
surface  of  the  chest  carefully  inspected,  more  especially  those 
parts  which  are  superficial  to  the  course  of  the  aorta,  and  at 
which  the  vessel  comes  nearest  to  the  surface  (the  sternal  end 
of  the  second  right  interspace  in  particular).  But  in  order 
that  this  and  other  points  connected  with  the  physical  exami- 
nation of  the  thoracic  aorta,  and  the  symptomatology  of  its 
diseases,  may  be  thoroughly  understood,  it  will  perhaps  be 
well  for  me  to  describe  briefly  the  anatomical  course  of  the 
vessel  and  its  relations,  which  are  of  importance  from  a  prac- 
tical and  clinical  point  of  view. 

Aiiatoiiiical  course  and  relations  of  the  tlioracic  aorta. 

The  thoracic  aorta  arises  at  the  junction  of  the  third  left 
costal  cartilage  with  the  sternum,  i.e.  nearly  opposite  the 
point  of  union  of  the  upper  and  lower  sternal  regions,  and 
terminates  in  the  abdominal  aorta  beneath  the  pillars  of  the 
diaphragm,  or  more  exactly,  on  the  anterior  surface  of  the  last 
dorsal  vertebra.  The  thoracic  aorta  has  been  divided,  for 
descriptive  purposes,  into  two  portions — the  aortic  arch  and 
the  descending  thoracic  aorta. 

The  aortic  arch  is  described  as  consisting  of  three  parts — 
the  ascendi)ig,  transverse,  and  descending  portions. 

The  ascending  portion  of  the  aortic  arch  arises  from  the 
base  of  the  left  ventricle,  on  a  level  with  the  lower  border  of 
the  third  left  costal  cartilage,  at  its  junction  with  the  sternum, 
and  passes  upwards  and  to  the  right  until  it  reaches  the  upper 
surface  of  the  second  right  costal  cartilage  at  its  junction  with 
the  sternum  (occasionally  encroaching  upon  the  inner  edge  of 
the   first   interspace),   where   it    terminates   in   the    transverse 

P 


2  26  Diseases  of  the  Heart. 

portion.  For  the  greater  part  of  its  course  it  is  enclosed  in 
the  membranous  sac  of  the  pericardium.  In  the  first  part  of 
its  course  it  is  deeply  situated,  being  covered  by  the  root  of 
the  pulmonar\-  artery,  and  being  closely  related  posteriorly  to 
the  cavity  of  the  left  auricle.  After  emerging  from  under 
cover  of  the  pulmonary  artery,  it  comes  in  close  relation- 
ship with  the  sternum  and  second  right  costal  cartilage, 
being  separated  from  these  structures  by  the  sac  of  the  peri- 
cardium, the  cellular  tissue  and  fat  of  the  mediastinum,  and 
(when  the  lungs  are  expanded)  by  the  thin  anterior  margin 
of  the  lungs,  more  especially  of  the  right  lung.  The  supe- 
rior vena  cava  lies  in  contact  with  it  on  the  right  side  ;  the 
pulmonary  artery  diverges  from  it  on  the  left  side,  while  be- 
hind it  is  placed  the  root  of  the  right  lung.  The  cardiac 
plexus  and  many  of  its  branches,  as  they  proceed  to  their 
terminations  in  the  coronary  plexuses,  are  closely  related 
to  the  root  of  the  aorta.  This  is  a  connection  which  is  of 
great  practical  importance  ;  while  the  facts  that  the  co- 
ronary arteries  arise  from  the  root  of  the  aorta,  and  that 
the  root  of  the  aorta  is  directly  continuous  with  the  aortic 
valves,  and  therefore  with  the  heart,  are  points  the  import- 
ance of  which,  from  a  practical  clinical  point  of  view,  is  self- 
evident. 

TJie  transverse  portion  of  the  arch  of  the  aorta  commences 
at  the  junction  of  the  upper  edge  of  the  second  right  costal 
cartilage  with  the  sternum,  and  crosses  almost  horizontally 
through  the  upper  sternal  region,  on  the  level  of  the  first 
interspace,  passing  backwards  and  downwards  deeply  into 
the  chest.  The  transverse  portion  terminates  in  the  descend- 
ing portion  of  the  aortic  arch,  at  the  lower  border  of  the  left 
side  of  the  body  of  the  fourth  dorsal  vertebra. 

The  transverse  portion  of  the  aortic  arch  is  separated  from 
the  surface  of  the  front  of  the  chest  by  the  mediastinal  fat 
and  connective  tissue,  by  the  remains  of  the  thymus  gland, 
during  inspiration  by  a  small  portion  of  the  right  pleura  and 
anterior  border  of  the  right  lung,  and  by  the  left  pleura  and 
anterior  border  of  the  left  lung.  The  left  pneumo-gastric,  the 
left  phrenic  and  superficial  cardiac  nerves,  and  the  left  superior 


Anatomical  course  of  t/ie  thoracic  aorta.         227 

intercostal  vein,  cross  in  front  of  this  portion  of  the  vessel.  On 
the  right  side,  at  its  origin,  it  is  closely  related  to  the  superior 
vena  cava,  the  right  pneumo-gastric  and  phrenic  nerves.  From 
its  upper  convex  surface  arise  the  great  blood  vessels  destined 
for  the  head  and  neck  and  upper  extremities  (the  innominate, 
left  common  carotid,  and  left  subclavian  arteries),  and  in  close 
relation  with  its  upper  surface  lies  the  left  innominate  vein. 
In  the  concavity  beneath  its  lower  surface  the  bifurcation  of 
the  pulmonary  artery  and  the  cardiac  plexus  of  nerves  are 
situated ;  the  recurrent  branch  of  the  left  pneumo-gastric  winds 
round  the  concave  lower  surface  of  the  vessel  to  which  the 
obliterated  ductus  arteriosus  is  attached.  Posteriorly  the  trans- 
verse portion  of  the  arch  of  the  aorta  is  in  close  contact  with 
the  left  recurrent  laryngeal  nerve,  as  it  ascends  through  the 
thorax  to  the  neck,  with  the  trachea  and  bifurcation  of  the 
bronchi,  the  oesophagus,  thoracic  duct,  and  more  deeply  with 
the  bodies  of  the  vertebrae. 

The  descending  portion  of  the  aortic  arch  commences  at  the 
junction  of  the  bodies  of  the  fourth  and  fifth  dorsal  vertebra;, 
and  passes  downwards  in  close  contact  with  the  left  side  of  the 
body  of  the  fifth  dorsal  vertebra,  until  it  terminates  at  the  lower 
end  of  the  body  of  that  vertebra,  in  the  descending  thoracic 
aorta. 

The  descending  thoracic  aorta  passes  downwards  in  contact 
with  the  spinal  column  ;  in  the  upper  part  of  its  course  it  lies 
on  the  left  side,  in  the  lower  part  of  its  course  on  the  anterior 
surface  of  the  bodies  of  the  vertebra;.  It  terminates  in  the 
abdominal  aorta  at  the  level  of  the  twelfth  dorsal  vertebra. 
On  the  right  side  of  the  vessel  lie  the  thoracic  duct  and  the 
large  azygos  vein.  On  the  left  side  the  vessel  is  covered  by 
the  left  pleura  and  left  lung.  In  front  of  it  are  placed  the 
root  of  the  left  lung  and  the  posterior  surface  of  the  peri- 
cardium, and,  therefore,  the  posterior  surfaces  of  the  left 
auricle  and  left  ventricle.  The  oesophagus  is  at  first  on  the 
left  side  of  the  aorta,  lower  down  it  makes  its  way  in 
front  of  the  vessel.  At  its  termination  the  thoracic  aorta 
is  enclosed  in  the  opening  formed  by  the  crura  of  the  dia- 
phragm. 


2  28  Diseases  of  the  Heart. 

In  health,  inspection  gives  no  information  as  to  the  condi- 
tion of  the  thoracic  aorta  ;  in  other  words,  neither  pulsation 
nor  prominence  can  be  seen  on  those  parts  of  the  surface  of 
the  chest  which  correspond  to  the  position  of  the  vessel  under- 
neath. When,  however,  the  vessel  is  diseased,  more  especially 
when  it  is  affected  with  aneurismal  dilatations,  local  promin- 
ence and  pulsation  at  the  part  of  the  chest,  corresponding  to 
the  position  of  the  aneurismal  dilatation,  are  often  observed. 
In  order  to  detect  slight  elevations  of  the  chest  wall  and 
slight  pulsations,  a  special  method  of  inspection  is  neces- 
sary ;  instead  of  placing  himself  in  front  of  the  patient 
and  looking  straight  on  to  the  surface  of  the  chest,  the  ob- 
server should  place  himself  at  one  side  of  the  patient — the 
opposite  side  to  that  from  which  the  rays  of  light  are  pro- 
ceeding— -and  should  then  bring  his  eye  to  the  same  hori- 
zontal plane  as  the  surface  of  the  chest  which  he  wishes  to 
examine.  If  the  illumination  is  good,  slight  elevations  and 
pulsations,  which  might  easily  escape  observation  by  the  or- 
dinary or  full-face  method  of  inspection,  can  b}'  this  means 
be  readily  detected. 

The  most  frequent  position  for  aneurismal  or  aortic  pulsa- 
tion is  the  second  right  interspace  close  to  the  sternum  ;  for, 
in  the  first  place,  the  ascending  portion  of  the  aortic  arch  is 
more  liable  to  be  affected  by  aneurismal  dilatation  than  any 
other  part  of  the  vessel  ;  and,  in  the  second,  comparatively 
small  aneurisms  are  apt  to  produce  bulgings  at  this  spot,  for 
the  aorta  is  here  very  superficial.  Aneurisms  may,  however, 
affect  the  vessel  in  any  part  of  its  course,  and  may  'point' 
at  any  part  of  the  chest  with  which  the  dilated  vessel  comes 
in  contact.  Further  details  on  these  points  will  be  afterwards 
given.     (See  Chapter  VIII.) 

In  some  cases  of  aortic  dilatation  and  aneurism,  pulsation 
is  seen  in  the  supra-sternal  notch. 

PALPATION  APPLIED  TO  THE  EXAMINATION  OF  THE 
THORACIC  AORTA. 

In  health  the  pulsation  of  the  aorta  can  sometimes  be 
felt    in    the    supra-sternal    notch,    but    in    no    other    position. 


Percussion  of  t lie  thoracic  aorta.  229 

When  the  vessel  is  dilated,  more  especially  when  a  saccular 
aneurism  is  in  contact  with  the  chest  wall,  pulsation  can  often 
be  felt  over  the  position  of  the  sac.  When  the  chest  wall  is 
bulged  forwards,  the  alteration  in  level  can  often,  of  course, 
be  detected  by  the  finger  as  well  as  by  the  eye. 

To  detect  slight  superficial  pulsations  (those  pulsations, 
for  example,  which  are  produced  by  an  aneurismal  sac 
which  is  in  contact  with  the  chest  wall,  but  which  has  not  as 
yet  produced  perforation  or  prominence),  the  fingers  of  the 
right  hand  should  be  lightly  placed  over  the  seat  of  the 
suspected  dilatation.  In  some  cases  in  which  the  aneurism 
is  deeply  seated,  and  in  which  there  is  no  superficial  pulsation, 
forcible,  deep-seated  and  expansile  pulsation  can  sometimes 
be  detected  by  forcibly  compressing  the  chest  during  expira- 
tion, between  the  two  palms,  one  hand  being  placed  on  the 
front  and  the  other  on  the  back  of  the  chest. 

When  the  transverse  portion  of  the  arch  is  dilated  or 
aneurismal,  pulsation  can  often  be  very  readily  felt  in  the 
supra-sternal  notch, — the  head  should  be  bent  well  forwards  so 
as  to  relax  the  sterno-mastoids,  and  the  forefinger  of  the  right 
hand  placed  in  the  supra-sternal  notch,  and  pushed  down- 
wards behind  the  manubrium  sterni. 

Vibratile  thrills  can  be  felt  over  the  course  of  the  aorta, 
more  especially  over  the  position  of  the  ascending  portion  of 
the  aortic  arch,  in  some  cases  of  dilatation  and  aneurism. 

PERCUSSION  APPLIED  TO  THE  EXAMINATION  OF  THE 
THORACIC  AORTA. 

Percussion  of  the  healthy  aorta  }aelds  only  negative  re- 
sults. At  its  origin  the  vessel  is  overlapped  by  the  pulmonary 
artery,  and  even  when  the  percussion  note  is  impaired  over 
the  part  of  the  chest  corresponding  to  the  root  of  the  aorta, 
as  it  is,  for  example,  in  very  full  expiration,  the  dulness  is  of 
course  derived  from  both  vessels.  After  the  aorta  emerges 
from  under  cover  of  the  pulmonary  artery,  although  it  lies 
close  under  the  sternum,  its  position  and  outline  in  health 
cannot  be  definitely  determined  by  means  of  percussion,  for 
on    percussion    over    the    manubrium    sterni    in    the    healthy 


230  Diseases  of  the  Heart. 

condition,  a  n:iore  or  less  resonant  note  is  obtained.  In  the 
subsequent  part  of  its  course  the  vessel  is  so  deeply  situated 
as  to  preclude  the  possibility  of  detecting  its  presence  by  this 
means  of  investigation. 

When  the  aorta  is  dilated  or  affected  with  aneurism,  per- 
cussion often  yields  most  important  results  ;  the  extent  and 
position  of  the  dulness  depend,  as  we  shall  afterwards  see, 
upon  the  size  and  position  of  the  sac,  more  especially  upon 
its  relation  to  the  lung  and  to  the  chest-wall.  The  percussion 
resistance  is  often  increased  over  a  dilated  or  aneurismal 
aorta,  the  resistance  being  greatest  in  those  cases  in  which  an 
aneurismal  sac,  filled  with  laminated  clot,  lies  in  close  con- 
tact with  the  chest  wall. 

AUSCULTATION  APPLIED  TO  THE  EXAMINATION  OF  THE 
THORACIC  AORTA. 

In  health  two  sounds  can  usually  be  heard  when  the 
stethoscope  is  placed  over  the  course  of  the  thoracic  aorta. 
Over  the  ascending  portion  of  the  aortic  arch  these  sounds 
closely  resemble  the  normal  heart  sounds,  only  that  they 
are  less  loud,  the  first  sound  more  especially  being  weaker  than 
the  first  sound  as  heard  over  the  heart  itself  Over  the 
descending  portion  of  the  thoracic  aorta  the  sounds  are  usually 
very  faint  and  distant. 

The  sounds  heard  over  the  aorta  undergo  the  same  quan- 
titative and  qualitative  alterations,  which  have  previously  been 
described  in  detail  in  treating  of  the  modifications  of  the 
cardiac  sounds  ;  and  since  the  sounds,  which  are  heard  over 
the  aorta,  more  especially  those  heard  over  the  ascending 
and  transverse  portions  of  the  aortic  arch,  are  for  the  most 
part  composed  of  the  sounds  produced  within  the  heart, 
propagated  through  the  aorta  to  the  ear  of  the  observer,  it 
follows,  that  alterations  of  the  heart  sounds  (more  particularly 
those  alterations  which  are  due  to  disease  of  the  aortic  valves), 
will  be  heard  over  the  course  of  the  aorta.  In  other  words,  it 
is  essential  to  remember  that  murmurs  heard  over  the  aorta 
are  very  frequently  due  to  disease  of  the  cardiac  valves,  and 
not  to  disease  of  the  aorta. 


Ansailtation  of  the  tJioracic  aorta.  231 

Alterations  of  the  sounds  heard  over  the  aorta  (both  quan- 
titative and  quahtative  modifications)  may,  however,  be  due 
to  disease  of  the  aorta  itself;  and  in  cases  of  this  description, 
the  heart  sounds,  as  heard  over  the  heart  itself,  may  be  per- 
fectly normal.  When,  for  example,  an  aneurism  of  the  aorta 
approaches  the  surface  of  the  chest,  the  aortic  or  cardiac 
sounds  are  much  more  clearly  and  distinctly  heard  over  that 
part  of  the  chest,  which  corresponds  to  the  position  of  the 
aneurism,  than  they  would  be  under  normal  circumstances. 
In  some  cases,  the  change  is  merely  a  quantitative  one  ;  in 
others,  a  murmur  is  heard.  But  I  must  defer  the  more  de- 
tailed description  of  the  character  of  the  sounds  in  cases  of 
this  nature  until  I  come  to  treat  of  aneurismal  and  other 
dilatations. 

In  other  cases  in  which  the  aorta  itself  is  healthy,  the 
aortic  sounds  appear  to  be  louder  than  in  health,  in  conse- 
quence of  the  fact  that  they  are  more  easily  conducted  to  the 
ear  than  in  the  normal  condition.  When,  for  example,  a  solid 
tumour  lies  in  contact  with  the  aorta  on  the  one  hand  and 
with  the  chest  wall  on  the  other,  an  apparent  increase  of  this 
description  is  frequently  observed.  On  the  other  hand,  ap- 
parent diminution  is  produced  by  all  those  conditions,  such  as 
emphysema,  for  example,  which  interfere  with  conduction.  I 
need  not,  however,  go  into  details  with  regard  to  these  points, 
but  must  refer  the  reader  to  what  has  been  already  stated 
with  regard  to  the  modifications  of  the  heart  sounds. 

When  the  aorta  is  compressed  and  constricted,  a  systolic 
murmur  may  be  generated. 

THE    EXAMINATION    OY   THE    PERIPHERAL   ARTERIES. 

In  all  cases  of  cardiac  and  arterial  disease  it  is  of  the 
greatest  importance  to  observe  the  condition  of  the  peripheral 
and  superficial  arteries,  and  to  ascertain  the  manner  in  which 
the  circulation  is  being  carried  on  in  these  vessels. 

By  observing  the  colour  of  the  skin  we  obtain  important 
information  as  to  the  condition  of  the  peripheral  circulation 
(both  arterial  and  venous),  but  this  point  has  been  already 
considered  in  treating  of  the  physiognomy  of  cardiac  cases. 


232  Diseases  of  the  Heart. 

The  radial  is  the  artery  which  is  usually  examined,  but 
the  condition  of  the  carotids,  temporals,  brachials,  etc.,  and 
the  character  of  the  pulse  in  these  vessels  should  also  be 
noted. 

I  mustj  therefore,  now  describe  the  manner  in  which  we 
observe  the  pulse  and  the  characters  which  it  presents  both  in 
health  and  disease.  And  in  order  that  the  subject  may  be 
thoroufjhly  understood  (for  it  must  be  remembered  that 
important  modifications  of  the  pulse  are  met  with  independ- 
ently of  any  cardiac  or  arterial  disease)  I  shall  take  a  some- 
what comprehensive  view  of  the  subject,  and  shall  not  limit 
the  description  altogether  to  the  alterations  which  are  met 
with  in  disease  of  the  heart  and  aorta. 

THE  EXAMINATION  OF  THE  PULSE,  INCLUDING  A 
DESCRIPTION  OF  THE  SPHVG.MOGRAPH. 

At  each  contraction  of  the  left  ventricle,  some  five  or  six 
ounces  of  blood  are  suddenly  propelled  into  the  aorta,  and  a 
blood-wave  is  generated,  which  is  rapidly  propagated  through 
the  arterial  system.  The  temporary  distention  of  the  arterial 
walls  which  is  caused  by  this  blood-wave,  can  be  felt  by  the 
finger  or  measured  by  the  sphygmograph,  and  is  termed  the 
pulse. 

The  exact  character  of  the  arterial  expansion,  i.e.  of  the 
pulse,  varies  in  different  cases,  and  depends  partly  upon  the 
mode  of  contraction  of  the  left  ventricle,  and  the  amount  of 
blood  which  it  propels  into  the  aorta,  and  partly  upon  the 
condition  of  the  arterial  system.  It  is  evident  therefore  that 
in  the  examination  of  the  pulse  we  have  an  important  means 
of  investigating  tJie  condition  of  the  heart  and  of  the  arterial 
system  ;  and  since  the  condition  of  the  arterial  system  is  to 
a  large  extent  regulated  by  the  vaso-motor  nerve  apparatus, 
we  are  enabled,  by  the  observation  of  the  pulse,  to  obtain  in 
many  cases  valuable  information  as  to  the  condition  of  the 
nerve  tone  {i.e.  the  general  tone  of  the  system);  the  frequency 
and  strength  of  the  pulse  being  chieflly  vauable  in  this  respect. 

'  Text- Booh  of  Physiology,  by  Professor  .M.  Foster,  p.  157. 


The  Examination  of  iJie pulse.  233 

The  radial  is  the  artery  which  is  usually  examined,  and 
in  speaking  of  the  pulse  the  radial  pulse  is  meant ;  but,  in 
cases  of  cardiac  and  arterial  disease,  the  condition  of  other 
vessels  (the  carotids,  temporals,  brachials,  etc.)  should  be 
noted. 

MODE   OF   OBSERVIXG   THE    PULSE. 

We  observe  the  characters  of  the  radial  pulse  by  means 
of— 

(1)  the  finger  {palpation)  ; 

(2)  the  eye  {inspection)  ; 

(3)  the  sphygmograph. 

(l)   PALPATION,   OR   THE   EXAMINATION    OF   THE   PULSE 
BY   THE   FINGER. 

The  correct  observation  of  the  exact  characters  of  the 
pulse  by  the  finger  is  a  matter  of  extreme  difficulty,  and  is 
only  acquired  by  long  practice.  Since,  however,  it  is  the 
method  which  is  not  only  always  available,  but  which  yields 
far  more  useful  and  important  information  than  any  other,  the 
student  should  spare  no  pains  to  make  himself  master  of  it. 
Two  or  three  fingers  should  be  applied  over  the  artery 
where  it  becomes  superficial  at  the  lower  end  of  the  radius, 
and  the  condition  of  the  pulse  noted  as  regards — 

{a)  its  frequency  ; 

{b)  its  rhythm  ; 

(^)   its  volume  ; 

{d)  its  compressibility  or  tension  ; 

{e)  the  special  characters  of  each  pulse  wave  (celerity, 
dicrotism,  etc.)  ;  the  condition  of  the  vessel  (in 
respect  to  its  fulness)  during  the  diastole  of 
the  ventricle,  i.e.  between  the  beats  ; 

(/)  the  condition  of  the  arterial  coats. 

{g)  la  cases  of  suspected  aneurism  or  intra-thoracic 
tumour  a  comparison  of  the  two  radial  pulses 
should  be  made. 


234  Diseases  of  the  Heart. 

(2)    INSPECTION   OF   THE   PULSE. 

In  well-nourished  individuals  the  radial  pulse  is  hardly,  if  at 
all,  visible  when  the  circulation  is  tranquil ;  but  in  emaciated 
subjects,  and  during  cardiac  excitement,  its  pulsation  can 
often  be  distinctly  seen.  Pulsation  is  very  visible  in  certain 
cases  of  disease,  notably  in  conditions  of  high  tension;  in 
atheroma,  where  the  artery  stands  out  as  a  rigid,  tortuous 
cord ;  and  in  aortic  regurgitation,  where  the  pulsation  is 
visible,  jerking,  and  collapsing,  and  the  artery  tortuous  (the 
locomotive  pulse). 

In  conditions  of  vaso-motor  relaxation  with  excited  action 
of  the  heart,  the  pulse  in  the  peripheral  vessels  (the  radial  for 
example)  may  present  the  visible,  jerking,  collapsing  character 
of  aortic  regurgitation  ;  but  the  marked  (visible,  jerking,  col- 
lapsing) pulsation  in  the  large  vessels,  e.g.  the  carotids,  which 
is  60  characteristic  of  aortic  regurgitation,  is  not  observed. 


(3)   THE   EXAMINATION    OF   THE   PULSE   BY    MEANS 
OF   THE   SPHYGMOGRAPH. 

The  exact  characters  of  the  pulse,  i.e.  of  its  individual 
waves,  and  of  their  relationship  to  one  another,  are  graphically 
demonstrated  by  means  of  the  sphygmograph.  The  instru- 
ment is  chiefly  useful  as  an  indicator  of  the  manner  in  which 
the  circulation  is  being  carried  on,  and  of  the  general  con- 
dition of  the  vascular  system  ;  it  sometimes  gives  im.- 
portant  diagnostic  evidence,  as  in  the  earlier  stages  of  chronic 
Bright's  disease  (especially  the  cirrhotic  kidney),  and  in  some 
aneurisms;  but  it  is  comparatively  useless  and  superfluous 
as  a  means  of  diagnosing  individual  cardiac  affections.  But 
although  its  (direct)  diagnostic  value  is  limited,  it  sometimes 
enables  us  to  form  a  more  correct  opinion  than  we  could 
otherwise  of  the  severity  of  a  lesion  or  case  ;  in  pneumonia, 
and  typhoid  fever  for  example,  it  may  afford  most  useful 
prognostic  information,  and  the  same  may  be  said  of  many 
cardiac  affections.     I  must  repeat,  however,  that  the  examina- 


Sphygmogi'aphic  examination  of  the p2ilse.       235 

tion  of  the  pulse  by  means  of  the  sphygmograph  is  altogether 
secondary  and  subordinate  to  the  ordinary  examination  by  the 
finger. 

FORMS    OF    SPHYGMOGRAPH. 

Mahomed's  modification  of  Marey's^  Sphygmograph,  and 
Dudgeon's^  Sphygmograph,  are  the  best  forms.  (Dr  W.  J. 
Fleming  of  Glasgow  introduced  a  'simple  form  of  transmis- 
sion sphygmograph'  some  years  ago.  I  have  not  had  an 
opportunity  of  using  this  instrument,  which  is  described  and 
figured  in  the  Journal  of  Anatoviy  and  Pliysiology,  vol.  xii. 
p.  144). 

For  home  practice  or  hospital  work  I  prefer  Mahomed's 
modification  of  Marey's  instrument,  as  I  think  it  permits  of 
more  accurate  adjustment  of  the  pressure  ;  but  for  general 
practice  Dudgeon's  instrument  is  undoubtedly  most  con- 
venient ;  it  is  extremely  portable,  easily  applied  in  any 
position  of  the  patient,  and  is  only  one-third  of  the  cost  of 
the  larger  instrument.  With  it  excellent  tracings  may  be 
obtained,  and  its  inventor  claims  that  it  gives  a  more 
accurate  and  natural  representation  of  the  up-stroke  than 
can  be  obtained  by  Marey's  instrument.^ 

'  This  instrument  is  made  by  Krohne  and  Sesemann,  8  Duke  Street,  Man- 
chester Square,  London. 

^  Dr  Dudgeon's  instrument  is  made  by  Mr  J.  Ganter,  and  may  be  obtained 
through  any  instrument-maker. 

'  Dr  Dudgeon  claims  the  following  advantages  for  his  instrument  : — 

r.  It  magnifies  the  movements  of  the  artery  in  a  uniform  degree,  viz.  50  times. 

2.  The  pressure  of  the  spring  can  be  regulated  from  i  to  5  ounces. 

3.  It  requires  no  wrist-rest,  and  may  be  used  with  equal  facility  whether  the 
patient  is  standing,  sitting,  or  lying. 

4.  With  it  a  tracing  of  the  pulse  can  be  made  almost  as  quickly  as  the  pulse 
can  be  felt  with  the  finger. 

5.  Its  sensitiveness  is  so  great  that  it  records  the  slightest  deviation  in  form  or 
character  of  every  beat. 

6.  Its  construction  is  so  simple,  that  if  accidentally  broken  any  watchmaker 
can  repair  it. 

7.  It  is  so  small  [2h  by  2  inches),  and  it  is  so  light  (4  oz. ),  that  it  can  easily 
be  carried  in  the  pocket. 

8.  It  is  only  one-third  of  the  price  of  the  imperfect  and  cumbrous  instruments 
hitherto  offered  (o  the  profession. 


236 


Diseases  of  J  he  Heart. 


DESCRIPTION   OF   THE   SPHYGMOGRAPH. 
MaJiomed's  modification  of  Mareys  Spliygviograph  consists 

of- 

I.  A  steel  spring,  A  (see  figs.  60,  61,  and  62),  which  rests 
on  the  artery,  and  which  moves  up  and  down  with  each 
movement  of  the  vessel. 

One  end  of  the  spring,  A'  (see  figs.  61  and  62),  is  so  attached  by  a 
hinge  to  the  framework  of  the  instrument  that  vertical  (up  and  down 
movement  is  alone  permitted.     To  the  under  surface  of  the  free  end  of 
the  spring  an  ivory  pad.  A",  is  fixed.     The  ivory  pad  rests  on  the  arter)-. 


Fig.  60. — Ma/ioiiied^s  Alodification  of  Mareyi's  Sphygmograph. 

A,  points  to  the  steel  spring  ;  A',  to  its  point  of  attachment  to  the  framework  ;  B, 
the  first  lever ;  B',  its  point  of  attachment  to  the  steel  spring  A ;  C,  the 
writing  lever  ;  C',  its  free  end,  which  carries  a  pen  ;  C",  its  point  of  attach- 
ment to  the  framework  ;  D,  the  screw  for  bringing  the  turned  up  free  end 
of  lever  B  in  contact  with  lever  C  ;  E,  the  screw  for  increasing  the  pressure  ; 
F,  the  dial  on  which  the  amount  of  pressure  is  indicated  ;  G,  the  slide  carry- 
ing the  strip  of  smoked  paper;  H,  the  clockwork,  which  is  wound  up  by  a 
screw  on  the  opposite  side  to  that  shown  in  the  figure  ;  I,  I,  parts  of  the 
instrument  over  which  the  straps,  which  fix  it  to  the  arm,  are  passed. 

2.  An  arrangement  of  levers,  by  means  of  which  the  move- 
ments of  the  steel  spring  {i.e.  of  the  artery)  are  magnified 
and  recorded  on  a  piece  of  smoked  paper. 

There  are  two  levers.  The  lower  one,  B,  is  so  hinged  by  its  proximal 
end,  B',  to  the  middle  of  the  steel  spring,  that  up  and  down  mo\ement 
is  alone  permitted.     The  free  end  of  this   lever   iB",  figs.  61   and  62)   is 


The  SphyginoQ^rapJi. 


237 


turned  up  at  a  right  angle,  and  ends  in  a  rounded  or  knife-shaped  edge. 
Through  the  free  extremity  of  this  lever,  B  (just  before  it  terminates  in 
the  turned  up  end,  B"),  a  screw  D  is  passed.  The  point  of  the  screw  is 
always  (by  the  force  of  gravity)  in  contact  with  the  steel  spring,  which  rests 
on  the  artery.  And  since  the  screw  D  and  the  lever  B  are  practically  the 
same,  it  follows  that  every  mo\ement  of  the  artery  is  of  necessity  com- 
municated to  the  turned  up  extremity  B",  of  the  lever  B.  The  object  of 
the  screw  D  is  to  raise  or  lower  the  turned  up  edge  of  the  lever  B,  so 
that  it  may,  whatever  the  position  of  the  steel  spring,  be  in  proper  con- 
tact with  the  writing  lever  C,  in  other  words,  in  order  that  it  may  always 
communicate  the  movements  of  the  steel  spring,  i.e.  of  the  artery,  to 
the  writing  lever  C. 

The  second  lever,  C,  is  so  fixed  at  its  distal  end,  C",  to  the  frame- 
work of  the  instrument,  that  vertical  movement  is  alone  possible.  The 
free  end  of  this  lever,  C,  carries  a  pen  which  records  its  movements 
on  a  strip  of  smoked  paper  propelled  past  it  at  a  fixed  rate  by  means 
of  clockwork.  In  order  that  the  movements  of  the  steel  spring  may  be 
communicated  to  the  writing  lever,  the  knife-edge  of  lever  B  must  be  in 
contact  with  lever  C,  as  shown  in  figure  61.  This  is  effected,  as  has  been 
already  stated,  b\'  alteration  of  the  screw  D. 


Fh;.  61.  Fig.  62. 

Fig.  61.— Scheme  showing  the  essential  parts  of  the  instrument  7vhen  in  -woi-king 
ordet — i.e.  the  turned  up  knife-edge  B"  of  the  short  lever  in  contact  with 
the  writing  lever  C.     Every  movement  of  the  steel  spring,  at  A",  i.e.  of 
the  artery,  will,  when  the  knife-edge,  B",  is  in  this  position,  be  communicated 
to  the  writing  lever.     The  letters  have  the  same  significance  as  in  fig.  60. 
N.B. — (The  framework  of  the  instrument  has  been  removed). 
Fig.  62. — Scheme  showing  the  essential   parts  of  the  instrument    after  increase 
of  the  pressure.      The   knife-edged   B"  is  no  longer    in   contact    with  the 
writing  lever,  and  the  movements  of  the  steel  spring  A",  i.e.  of  the  artery, 
are  no  longer  communicated  to  it.     In  order  to  put  the  instrument  into 
working  order  the  knife-edge  B"  must  be  raised  to  the  position  indicated  by 
the  dotted  lines.     This  is  effected  by  means  of  the  screw  D. 
3.  An   arrangement    by   which    the    amount    of   pressure 
exerted  by  the  steel  spring  on  the  artery  can  be  regulated 
and    measured.      This    is     a     most     important    part    of  the 
instrument,  and  is  the  modification  made  by  Mahomed.     It 
consists  of  an  eccentric,  E,  by  depression  of  which,  as  shown 
in  fig.  62,  a  definite  degree   of  pressure   can  be  made  upon 


2:;8 


Diseases  of  the  Heart. 


the  steel  spring.  The  amount  of  pressure  exerted  is  shown 
on  a  dial  (F,  in  fig.  6o)  in  ounces  troy.  The  eccentric  (see 
figs.  60, 6 1, 62)  is  depressed  by  turning  the  screw  E  (see  fig.  60). 

4.  A  clockwork,  H,  which  propels  at  a  fixed  rate  a  slide 
G,  to  which  a  strip  of  smoked  paper  is  attached. 

5.  A  framework  to  which  the  various  parts  of  the  in- 
strument are  fixed,  and  by  means  of  which  the  instrument  is 
fastened  to  the  arm  by  straps  (K,  K,  fig.  65). 

Dudgeon's  Pocket  SpJiygmograpJi  (see  fig.  63)  consists  of: — 

I.  A  steel  spring,  A  (see  fig.  64),  which  rests  upon  the 
artery,  and  moves  up  and  down  with  each  movement  of  the 
vessel. 

One  end  of  the  spring  (a)  is  tirmly  attached  to  the  framework  of  the 
instrument,  the  other  (C)  is  turned  up  at  a  right  angle.  To  the  under 
extremity  of  the  steel  spring  a  button,  B,  which  rests  on  the  arterj-, 
is  fixed  ;  and  to  the  turned  up  extremity  C  a  short  rod  (D)  is  firmly 
attached. 


Fig.  63. — Dudgeon's  Sphygmograph. 

2.  An    arrangement    of  levers    by    means    of  which    the 
movements     of    the    steel    spring,     i.e.    of    the    arter\-,    are 


The  Sphymograph.  239 

magnified  and  recorded  on  a  strip  of  smoked  paper  propelled 
by  clockwork. 

At  right  angles  to  D,  and  connected  with  it  by  the  axle  E,  rises  the 
upright  stem  F.  Every  upward  movement  of  the  steel  spring  causes 
the  upright  F  to  mo\-e  forwards.  At  the  top  of  F  is  a  loop  in  which  a 
rod  K  lies.  This  rod  is  connected  at  the  axle  H  with  a  bent  rod  having 
a  counterpoise  I.  When  the  upright  F  makes  a  forward  movement, 
the  oblique  rod  K  also  swings  forwards  by  the  weight  of  its  counterpoise. 

To  the  lower  end  of  K  the  needle  L  is  attached  by  the  hinge  M,  and 
its  point  describes  on  the  smoked  paper,  which  is  propelled  by  the 
clockwork  machinery  at  a  uniform  velocity,  a  graphic  representation  of 
the  movements  communicated  to  it. 


Fig.  64.  —  Scheme  showing  the  different  parts  of  Dudgeon's  Sphygmograph. 
The  description  of  the  figure  is  given  in  the  text. 

3.  An  eccentric,  by  means  of  which  the  pressure  can  be 
increased  from  one  to  five  ounces. 

4.  A   clockwork,  by  means   of  which   a   strip  of  smoked 
paper  is  propelled  at  a  fixed  rate  under  the  writing  lever. 

5.  A  framework,  by  means  of  which  the  instrument  can 
be  attached  to  the  arm.^ 

'  For  further  particulars  respecting  Dr  Dudgeon's  instrument,  see  his  book, 
The  Sphygmograpli  ' 


!40 


Diseases  of  the  Heart. 


DIRECTIONS   FOR   TAKING   A   SPHYGMOGRAPIIIC   TRACING 
WITH    MAREY'S   instrument.^ 

I.  Place  the  Patient  in  proper  position. —  He  should  be 
seated  by  the  side  of  a  low  tabic,  his  arm  resting  on  the  pad 
(a  double  inclined  plane),  as  represented  in  fig.  65,  the  fingers 
semiflexed  into  the  palm. 

If  the  fingers  are  quite  extended  the  arterj'  is  too  much  stretched, 
and  jerking  movements  of  the  tendons,  which  interfere  with  the  tracing, 
are  apt  to  occur.  If  the  fingers  are  quite  flexed,  the  rigidity  of  the 
tendons  prevents  the  perfect  appHcation  of  the  instrument. 

The  position  should  be  as  easy  as  possible,  for  it  is  essential  that 
the  arm  be  kept  at  perfect  rest.  The  shirt  sleeve  should  be  turned  up  ; 
and  it  must  be  loose,  lest  it  interfere  with  the  circulation  through  the 
arm. 

C 


Fig.  65. — Marey's  Sphygmograph  applied  to  the  wrist. 

2.  Mark  the  exact  position  of  the  artery  ivitJi  ink  or  pejieil. 
— The  ink  line  should  be  prolonged  to  the  ball  of  the  thumb, 
i.e.  below  the  instrument  when  ///  situ.  By  this  means  we 
can,  without  removing  the  sphygmograph,  ascertain  if  the 
ivory  pad  is  still  in  proper  position,  i.e.  exactly  over  the 
artery. 

'  For  further  information  on  the  subject  the  student  is  referred  to  Dr  Ma- 
homed's papers  in  the  Irlcdical  Times  and  Gazette  (January  20th,  1872,  and  fol- 
lowing numbers),  and  in  Gant's  Surgery  (vol  i.,  page  52),  to  which  I  am  indebted 
for  much  of  my  information  on  the  subject,  and  from  which  some  of  the  following 
lules  for  the  application  of  the  instrument  are  derived. 


JMarcy's  SphygmograpJi.  241 

Before  applying  the  sphygmograph,  the  harmless  nature 
of  the  procedure  must  be  explained  to  the  patient,  for  it  is  of 
the  greatest  importance  to  avoid  anything  which  will  excite 
or  disturb  the  action  of  the  heart.  Some  persons  become 
considerably  agitated,  thinking  that  an  operation  is  about  to 
be  performed.  (One  of  my  patients  left  the  hospital  rather 
than  have  the  instrument  applied.)  In  such  cases  a  pre- 
liminary application  to  a  fellow-patient  or  nurse  is  advisable. 

3.  Apply  the  ifistminent,  having  previously  screwed  up  the 
clockwork  and  placed  the  pressure  at  zero. — The  ivory  pad 
must  be  accurately  applied  over  the  very  centre  of  that  part  of 
the  artery  which  lies  at  the  inner  side  of  the  styloid  process 
of  the  radius.  By  compressing  the  vessel  at  this  spot,  where 
it  is  superficial  and  rests  upon  bone,  we  can  be  quite  certain 
that  the  entire  pressure  of  the  spring  will  be  exerted  upon  it. 
The  instrument  is  then  firmly  strapped  to  the  arm.  The 
straps  should  be  unyielding — not  elastic.  The  slide  carrying 
the  strip  of  smoked  paper  is  next  to  be  fitted  into  the  frame, 
Care  must  be  taken  that  the  paper  is  firmly  and  evenly 
stretched.  This  is  best  efi'ected  by  first  accurately  fitting  it 
and  doubling  its  edges  over  the  frame,  then  removing  and 
smoking  it  over  a  piece  of  burning  camphor,  and  finally 
fitting  it  to  the  frame  again.  The  paper  should  not  be  over- 
smoked, and  the  point  of  the  pen  must  not  press  too  heavily 
against  it,  or  friction  will  prevent  free  movement,  and  the 
tracing  will  be  imperfect. 

4.  Adjust  the  pen. — The  point  of  the  pen  is  then  (by 
means  of  the  screw  D,  see  figs.  60  and  62)  to  be  brought 
level  with  the  centre  of  the  strip  of  smoked  paper,  as  shown 
in  figs.  60  and  65. 

5.  Regulate  the  presstire  by  means  of  the  screw  L,  until 
the  maximum  amount  of  movement  of  the  writing  lever  is 
obtained.^  There  is  a  certain  pressure,  depending  upon  the 
am.ount  of  expansion  which  is  going  on  in  the  artery,  at 
which  the   tracing   is  best  marked.     If  the  pressure  is  too 

'  The  reader  must  not  forget  that  every  alteration  of  the  pressure,  i.e.  every 
alteration  in  the  position  of  the  steel  spring  necessitates  a  fresh  adjustment  of  the 
writing  lever  by  means  of  the  screw  D. 


242  Diseases  of  the  Heart. 

little,  i.e.,  if  the  steel  spring  just  touches  the  artery  in  its  ex- 
panded state,  the  rise  of  the  lever  will  be  insignificant ;  if,  on 
the  other  hand,  the  pressure  be  too  great,  the  artery  cannot 
expand  to  its  full  amount,  and  the  tracing  will  be  imperfect, 
— the  up  stroke  shortened  (see  fig.  66),  and  the  perfect 
development  of  tiie  secondary  waves  of  the  tracing  interfered 
with. 


Fig.   66. —  Tracing  taken  iinaer  too  great  pressure. 
The  up-stroke  is  cut  short,  and  the  perfect  development  of  the  tracing  prevented. 

If  the  tracing  is  satisfactory,  the  name  of  the  patient,  the 
date,  the  nature  of  the  disease,  and  the  amount  of  pressure 
which  is  required  for  {a)  the  perfect  development  of  the 
tracing,  and  {b)  the  complete  obliteration  of  the  pulse  in  the 
artery  (the  latter  being  the  gauge  of  the  strength  of  the 
pulse)  should  be  inscribed  upon  the  slip  of  smoked  paper  by 
means  of  a  needle  or  other  fine-pointed  instrument,  and  the 
tracing  rendered  permanent  by  dipping  it  in  a  rapidly  dr}-ing 
varnish.^ 

Character  of  a  good  tracing. — In  a  good  tracing  the  apex 
(b,  fig.  67)  is  pointed  ;  and  the  best  tracing  is  that  in  which  the 


Fig.   67. — A^or-nal  Piilsc  J  racing. 

up-stroke  is  tallest  and  the  apex  most  pointed.     It  occasionally 
happens  that   the  apex   is   rounded,   as   in   some  aneurisms 

'  The  varnish  recommended  by  Mahomed  is  made  by  macerating  an  ounce  of 
gum  benzoin  in  five  ounces  of  rectified  spirit ;  the  mixture,  which  should  be 
frequently  agitated,  is  allowed  to  stand  for  two  days,  and  the  clear  liquor  then 
poured  off  from  the  insoluble  constituents  of  the  gum.  Dr  Dudgeon  uses  the 
crystal  varnish  of  photographers,  or  a  varnish  consisting  of  one  ounce  of  gum 
damar  and  six  ounces  of  rectified  benzoline 


Marey's  Sphyginograph. 


243 


(see  figs.  68  and  69),  and  in  a  few  cases  of  aortic  stenosis 
(see  fig.  70) ;  but  this  is  so  extremely  rare,  that  a  tracing  in 
which  the  apices  are  rounded  should  always  be  regarded  as 
imperfect,  unless  it  has  been  verified  by  repeated  and  careful 
readjustments  of  the  instrument,  and  by  repeated  alterations 
of  the  pressure.^ 


Fig. 


Pressure  2.\  oz. 

68. — Aneuris7/i  of  Left  Axillary  Artery  {left  radial  tracing). — L.  G.,  set.  63, 
admitted  to  the  Newcastle  Infirmary  7th  March  1878,  with  a  large  aneurism 
of  the  left  axillary  artery.  The  apex  is  rounded  ;  all  the  curves  are 
obliterated. 


Pressure  3  oz. 
Fig.   69. — Aneu7-ism  of  Left  Subclavian  (left  radial  tracing). — J.  M.,  set.  50,  ad- 
mitted to  Newcastle  Infirmary  5th  September   1878  :  all  the  waves  in  the 
left  tracing  are  obliterated. 


Fit 


Pressure  l^  oz. 
70. — Aortic  Stenosis. — J.  B.,  set.  51,  admitted  to  Newcastle  Infirmary  29th 
November   1878,  suffering  from  anaemia  and  dropsy.     There  was  a  well- 
marked  aortic  systolic  murmur  ;  the  left  ventricle  was  not  hypertrophied. 
The  pulse  tracing  seems  to  show  that  the  murmur  was  organic. 


FiG.  71. — Pressure  i^  oz.  t'lG.    72. — Pressure  25   oz. 

Fig.  71. — Aortic  Stenosis  and  Dilated  Aorta. — J.  C,  puddler,  aet.  25,  admitted 
to  Newcastle  Infirmary  20th  February  1879.  The  patient  had  been  under 
observation  for  four  years  previously.  Marked  thrill  and  loud  systolic 
murmur  over  base  of  heart  and  over  aortic  region.  Heart  moderately 
hypertrophied.     Pressure  =  i|^  oz. 

Fig.  72.^ — Tracing  taking  from  the  same  patient  with  a  slightly  increased  pressure ; 
the  apex  is  now  pointed. 

'   In  most  cases  of  aortic   stenosis  a  pointed  apex  can    be   obtained   by  careful 
adjustment  and  regulation  of  the  pressure.      (See  figs.  71  and  72.) 


244  Diseases  of  the  Heart. 

Dr  Galabin  points  out  that  'if  the  tracing  of  any  pulse 
taken  at  a  low  pressure  show  a  very  marked  primary  summit, 
whose  proportionate  magnitude  is  modified  by  increase  of 
pressure,  then  the  tracing  taken  at  the  higher  pressure  more 
closely  represents  the  pulse-wave.  The  form  of  trace  at  the 
lower  pressure  may,  however,  have  much  significance,  and 
in  these  cases  the  whole  of  the  information  to  be  derived 
from  the  sphygmograph  cannot  be  compressed  into  one 
curve,  but  requires  at  least  two  for  its  expression,  namely, 
that  trace  which  has  the  greatest  amplitude,  and  another 
taken  at  a  higher  pressure.'^ 

The  cJiicf  points  to  be  attended  to  therefore  in  order  to  get  a 
perfect  tracing  are : 

(i)  The  accurate  adjustment  of  the  instrument,  and 

(2)  The  proper  regulation  of  the  pressure. 

The  following  tracings,  which  were  taken  consecutively 
from  the  same  pulse,  illustrate  the  eff"ects  of  different  degrees 
of  pressure. 

Speaking  generally  it  may  be  said  that  pulses  of  high 
tension  require  a  considerable  amount,  and  pulses  of  low 
tension  a  small  amount  of  pressure  for  their  perfect 
development.  But  to  this  general  rule  there  are  some  ex- 
ceptions. In  atheroma,  for  example,  the  amount  of  pressure 
required  to  obliterate  the  pulse  is  usually  considerable, 
the  arteries  are  abnormally  full,  but  the  condition  is  not 
necessarily  one  of  high  tension."  In  cases  of  atheroma  the 
development  of  a  pointed  apex  is  often  interfered  with,  unless 
a  small  amount  of  pressure  be  employed. 

I  n  comparing  the  tracings  from  diff"erent  arteries, — the  two, 
radials,  for  example, — a  procedure  which  is  desirable  in   all 

'  yoiirnal  of  Anatomy  and  Physiology,  vol.  x.  p.  306. 

*  In  the  first  edition  of  this  lecture  I  stated  that  the  pulse  in  atheroma  is  one 
of  low  tension.  This  is  not  always  the  case.  I  should  have  said,  that  for 
the  perfect  development  of  the  trace,  a  low  pressure  is  (as  a  rule)  required  ; 
and  that  the  amount  of  pressure  required  to  extinguish  the  pulse  in  atheroma  is 
not  a  criterion  of  the-  blood  pressure,  i.e.,  the  tension  of  the  pulse,  for  where  the 
vessel  is  rigid  a  considerable  amount  of  pressure  is  required  to  overcome  the 
resistance  of  the  arterial  wall,  and  it  is  only  after  the  rigidity  of  the  arterial 
wall  is  overcome  that  the  pressure  is  fully  exerted  upon  the  arterial  contents. 


Marey  's  Sphygmog raph . 


245 


cases  of  supposed  aneurism  or  solid  intra-thoracic  growth, 
the  best  obtainable  tracing  from  each  pulse  should,  in  the 
Jirst  place,  be  taken,  all  the  conditions  (with  the  exception  of 
the  pressure)  such  as  the  position  of  the  patient,  the  tight- 
ness with  which  the  instrument  is  strapped  to  the  wrist,  etc., 
being  so  far  as  is  possible  the  same  ;  and  in  this  connection 
it  is  very  important  to  remember  that  when  the  heart's  action 
becomes  excited  as  the  result  of  emotional  or  other  causes, 
the  character  of  the  tracing  may  be  materially  modified,  as  is 
shown  in  figs.  /T,,  74,  75,  and  '/6.  Tracings  slioiild,  tJierefore, 
always  be  taken  if  possible  during  tranquil  action  of  the  heart. 
In  the  second  place,  two  tracings  (one  from  either  radial) 
should  be  taken  with  all  the  conditions,  including  the  amount 
of  spring  pressure,  the  same. 


Fig.  73. — Pressure  2^  oz.  Fig.  74. — Pressure  2^  oz. 

Figs.  73  and  74 — Alterations  in  the  Pulse-tracing  as  ihe  result  of  Cardiac  Ex- 
citement.— A.  M.,  aet.  48,  admitted  to  the  Newcastle  Infirmary  suffering 
from  obscure  spinal  symptoms.  The  heart  became  excited,  and  the  tracing 
shown  in  fig.  74  was  taken  immediately  after  that  shown  in  fig.  73,  the 
instrument  in  the  meantime  remaining  in  situ.  The  spring  pressure  was 
the  same  in  each  case. 


KKl-vh 


Fig.  75. — Pressure  3  oz.  FiG.  79. — Pressure  3  oz. 

Figs.  75  and  76. — -Alterations  in  the  Pulse-tracing  -which  result  from  Cardiac 
Excitement. — Figs.  75  and  76  show  two  tracings  from  a  case  of  chlorosis. 
Case  :  E.  F.,  ret.  19,  admitted  to  Newcastle-on-T>Tie  Infirmary  3d  March 
1878.  The  tracing  shown  in  fig.  75  was  taken  on  8th  March  ;  the  tracing 
shown  in  fig.  76  was  made  three  minutes  later,  the  instrument  having  re- 
mained in  situ  ;  the  heart  had  become  excited.   Pressure  in  both  cases  =  3  oz. 


246 


Diseases  of  the  Heart. 


DIRECTIONS   FOR   THE   APPLICATION   OF   DUDGEON'S 
SPHYGMOGRAPH. 

Dr    Dudgeon    gives    the    following    directions    for    the 
application  of  his  instrument : — 

'  I.  Wind  up  the  clockwork,  used  to  drive  the  smoked  paper  along, 
by  means  of  the  milled  button  at  the  back  of  the  clockwork  box. 

'2.  Insert  one  end  of  the  smoked  paper  (smoked  side  uppermost)  on 
the  right-hand  side  of  the  instrument,  between  the  roller  and  small 
wheels. 

'3.  Make  the  patient  hold  out  either  hand  open  and  in  an  easy  posi- 
tion, the  fingers  pointing  towards  you  (see  fig.  ']'])^  and  direct  him  not 
to  move  the  wrist  or  fingers. 


Fig.   77 — Mode  of  apply iu^i^  Dudgeon's  Sphygviograph. 

'4.  Ascertain  the  precise  spot  where  the  radial  arterj'  beats  at  the 
wrist,  close  behind  the  eminence  of  the  os  trapezium. 

'  5.  Slip  the  band,  the  free  end  of  which  has  been  drawn  through  the 
clamp,  over  the  paitent's  hand. 

'6.  Apply  pressure  to  the  spring  by  turning  the  spring-regulator  so 
that  the  number  of  ounces,  or  portions  of  ounces,  you  wish,  is  pointed  to 
by  the  indicator.  The  pressure  may  be  altered  at  will  when  the  instru- 
ment is  fixed  on  the  arm. 


Dudgeons  Sphygviograph.  247 

'  7.  Place  the  bulging  button  of  the  spring  exactly  over  the  artery,  its 
long  axis  parallel  to  the  course  of  the  artery,  the  box  containing  the 
clockwork  resting  lightly  on  the  forearm  above. 

'8.  Retaining  the  instrument  in  its  place  with  the  left  hand,  draw 
the  band  through  the  clamp  with  the  thumb  and  forefinger  of  the 
right  hand,  holding  back  the  clamp  with  the  other  fingers  of  that  hand  ; 
when  the  requisite  tightness  has  been  obtained,  which  will  be  known  by 
the  point  of  the  needle  working  freely  over  the  centre  of  the  smoked 
paper,  screw  up  the  clamp  with  the  left  hand,  so  as  to  fix  the  in- 
strument. 

'9.  Set  the  smoked  paper  in  motion  by  pushing  towards  the  right  the 
small  handle  on  the  top  of  the  clockwork  box. 

'  10.  Let  the  paper  run  through,  and  do  not  touch  the  instrument  or 
the  patient,  unless  to  support  his  hand  in  your  own  right  hand,  to  secure 
perfect  steadiness. 

'  II.  Catch  the  paper  as  it  passes  out  of  the  instrument  in  your  own 
left  hand. 

'  12.  Stop  the  clockwork  as  soon  as  the  paper  has  passed.' — The 
Sphygmograph,  p.  67. 

Having  now  described  the  sphygmograph  and  its  mode 
of  application,  I  will  next  consider  the  characters  of  the 
normal  pulse  tracing,  and  the  modifications  which  occur  in  it. 

ANALYSIS    OF   A    SPHYGMOGRAPHIC    TRACING. 

A  pulse  tracing  consists  of  a  series  of  curves,  each  one  of 
which  corresponds  to  one  beat  of  the  pulse,  and  each  one 
of  which  corresponds  (in  time)  to  a  complete  cardiac  revolu- 
tion, i.e.,  the  time  which  elapses  from  the  commencement  of 
one  ventricular  systole  to  the  termination  of  the  ventricular 
diastole. 

Each  individual  pulse  curve,  a  to  a'  (fig.  ']i),  may  be 
artificially  divided  into  the  following  parts  : — 

1.  A  line  of  ascent  {a  to  b^. 

2.  An  apex  {b). 

3.  A  line  of  descent  {b  to  a'). 

This  division  is  convenient  for  descriptive  purposes,  but 
a  more  natural  division  is  that  which  separates  each  pulse 
wave  into  two  portions  (i  and  2,  fig.  78)  corresponding  in  time 
to  the  systole  and  diastole  of  the  left  ventricle  respectively. 

I  will  now  describe  each  of  these  different  parts. 


248  Diseases  of  tlic  Heart. 

The  line  of  asecnt  or  upstroke''  {a  to  b  fig.  'j'i)  represents 
the  sudden  distension  of  the  arterial  system  which  is  pro- 
duced by  the  contraction  of  the  left  ventricle  at  the  com- 
mencement of  the  ventricular  systole,  i.e.  when  the  aortic 
segments  are  suddenh'  opened. 

It  is  probably  also  partly  due  to  the  inertia  of  the 
instrument  ;  and,  in  some  cases,  as  in  atheroma  (where  the 
vessels  are  extremely  rigid),  to  impulse  or  shock. 


Pressure  3  oz. 
Fig.   78. — SpJivi^inographie  Tracittg  of  Norma!  Pti/se. — Male,  set.  25,  admitted   to 
the  Newcastle  Infirmary  suffering  from  psoriasis, 
(l.)  Line  of  ascent,  up-stroke  or  percussion  stroke  =  a  to  b.  (2,)  Apex  =  3. 

(3. )  Line  of  descent  =  ^  to  a';  d?=  aortic  or  dicrotic  wave ;  ^  =  aortic  notch;  ^  =  tidal 
wave.  A  B  =  base  or  respiratory  line.  l=Systolic  portion  of  the  tracing,  i.e. 
with  reference  to  the  systole  and  diastole  of  the  ventricle,  not  of  the  artery. 
2  =  Diastole  portion  of  the  tracing. 

(Note — Dr  Mahomed  tells  me  that  he  thinks  the  tidal  wave  in  this  tracing  is 
rather  too  sustained,  considering  the  amount  of  pressure,  viz.  3  oz.) 

The  direction  of  the  up-stroke  (whether  vertical  or  oblique) 
depends  (chiefly)  upon  : — 

1.  The  suddenness  of  the  ventricular  systole. 

2.  The  condition  of  the  aortic  segments. 

3.  In  some  degree,  the  facility  with  which  the  blood  wave 
is  propagated  from  the  base  of  the  aorta  to  the  radial  artery, 
and 

4.  The  condition  of  the  arterial  (radial)  coats. 

In  the  normal  tracing  the  up-stroke  is  nearly  vertical, 
for  the  contraction  of  the  ventricle  occurs  suddenly,  and 
there  is  no  undue  resistance  in  the  aortic  segments. 
When  the   ventricular  contraction   is   more   sudden   than  in 

'  It  is  belter,  I  think,  not  to  use  the  term  percussion  stroke,  proposed  by 
Mahomed,  for  unless  the  arteries  are  rendered  extremely  rigid  by  atheroma,  per- 
cussion or  shock  probably  takes  litt  le  or  no  part  in  the  produciion  of  the  up-stroke. 


Analysis  of  a  Sphygmographic  Tracing.         249 

health,  as  it  is,  for  example,  in  some  cases  of  aortic  regurgi- 
tation, and  in  conditions  of  cardiac  excitement,  the  up-stroke 
is  quite  vertical,  or  (in  tracings  taken  with  Marey's  instrument) 
it  may  even  slope  backwards.     (See  figs.  79  and  80.)^ 


Fig.  79. — Pulse-tracing  dn7-ing  Cardiac  Fig.  So. — Aortic  regurgitation. 

E.xcitement. 

Vice  versa  when  the  ventricular  contraction  is  slow  and 
hesitating, -as  in  some  cases  of  cardiac  debility;  when  the 
aortic  cusps  are  rigid  ;  when  the  arteries  are  obstructed 
either  by  internal  or  external  causes,  such  as  the  pressure 
of  a  tumour,  the  presence  of  an  atheromatous  patch  (at 
the  orifice  of  the  innominate  in  the  case  of  the  right  radial 
for  example)  ;  or,  when  a  globular  aneurismal  dilatation  is 
situated  between  the  heart  and  the  vessel  {i.e.  the  radial),  the 
up-stroke  may  be  oblique.     (See  figs.  81  and  82.) 


Pressure  \\  oz. 
Fig.  81. — Aortic  .Stenosis. — J.  B.,  Kt.  51,  admitted  to  Newcastle  Infirmary  29th 
November  1878,  suffering  from  anaemia  and  dropsy.  There  was  a  well- 
marked  aortic  systolic  murmur  ;  the  left  ventricle  was  not  hypertrophied. 
The  pulse-tracing  seems  to  show  that  the  murmur  was  organic,  and  not 
hsemic. 


Pressure  2\  oz. 
Fig.   82. — Aneurism  of  /eft  Subclavian. — ^J.  M.,  fet.   50,  admitted  to  Newcastle 
Infirmary  5th  September  1878  ;  all  the  waves  in  the  tracing  are  obliterated. 

'  In  cases  of  hypertrophy  of  the  left  ventricle  with  high  arterial  pressure,  the 
ventricular  contraction  may  be  laboured  and  prolonged  in  order  to  overcome  the 
obstruction,  but  the  commencement  of  the  contraction  is  sudden,  and  the  up-stroke 
veriicdl. 


250  Diseases  of  the  Heart. 

The  hcigJit  of  the  up-stroke  represents  the  degree  of  dis- 
tension of  the  vessel,  and  depends  upon — 

1.  The  force  and  (to  a  less  degree)  the  suddenness  with 
which  the  aortic  cusps  are  raised,  i.e.  upon  the  force  (_and  sud- 
denness) of  the  contraction  of  the  left  ventricle,  less  the  resist- 
ance offered  by  the  aortic  valve-cusps. 

2.  The  extensibility  of  the  arterial  coats,  which  in  its 
turn  depends  upon  the  condition  of  the  arterial  tunics 
(their  elasticity  or  rigidity),  and  the  state  of  the  vaso-motor 
system. 

3.  The  amount  of  compression  which  is  applied  to  the 
artery,  i.e.  the  spring  pressure  of  the  sphygmograph. 

The  up-stroke  is  tall  in  simple  nervous  palpitation,  and 
in  cases  in  which  a  large  amount  of  blood  is  suddenly  thrown 
into  the  arterial  system  by  a  hypertrophied  left  ventricle. 

In  free  mitral  regiirgitation  the  left  ventricle  may  be  considerably 
hypertrophied,  but  the  up-stroke  is  short,  for  in  such  cases  the  large  leak 
at  the  mitral  orifice  prevents  the  distention  of  the  arterial  system.  So, 
too,  in  Bright's  disease  and  atheroma,  a  powerful  (hypertrophied)  left 
ventricle  may  fail  to  produce  a  tall  up-stroke,  owing  to  the  unyielding 
condition  of  the  arterial  wall. 

Vice  versa,  the  up-stroke  is  sJwrt  where  the  left  ventricle  is 
weak  or  acting  feebly,  and  in  all  conditions  in  which  a  small 
amount  of  blood  is  being  pumped  into  the  arterial  system,  as 
in  aortic  stenosis  and  mitral  lesions. 

The  apex  of  tJic  tracing,  or  ^\-\q. primary  ventricular  luavc^ 
{b  in  fig.  yd>)  as  it  may  be  termed,  is,  in  the  great  majority  of 
tracings, — both  normal  and  pathological — pointed  ;  in  fact,  as 
I  have  previously  remarked,  a  rounded  apex  is  so  extremely 
rare,  that  any  tracing  in  which  the  apices  are  rounded  should 
be  regarded  with  suspicion,  and  should  never  be  accepted 
as  the  best  attainable  (most  perfect)  tracing  without  careful 
readjustment  of  the  instrument  and  alteration  of  the 
pressure. 

'   The  term  'percussion  wave''  is  applied  to  the  apex  by  Mahomed. 


Analysis  of  a  Sphygmogvapliic  Tracing.         251 

A  rounded  apex  does,  however,  occasionally  occur.  It  is 
met  with  in  some  aneurisms  ;  the  angles  of  the  pulse  curve 
are,  as  it  were,  flattened  out  (obliterated)  either  in  the  passage 
of  the  blood  wave  through  the  sac  of  the  aneurism,  or  by 
alterations  at  the  mouths  of  the  vessels  arising  from  the  sac, 
or  as  the  result  of  the  pressure  of  the  aneurismal  sac  on  the 
vessels  arising  from  it.  A  rounded  apex  is  also  seen  in  some 
cases  of  aortic  stenosis;  but  in  these  cases,  and  in  cases  of 
atheroma,  a  pointed  apex  can,  I  think,  usually  be  obtained 
by  accurate  adjustment  of  the  instrument  and  careful  regu- 
lation of  the  pressure. 

The  line  of  descent. — In  the  normal  pulse  tracing  the  line 
of  descent  {b  to  a'  in  fig.  78)  is  gradual,^  and  is  interrupted 
by  one  or  more  secondary  waves,  the  most  important  of 
which  is  the  dicrotic. 

The  direction  of  the  line  of  descent  depends  upon — {d)  the 
facility  with  which  the  blood  passes  out  of  the  arteries ; 
{b)  the  rapidity  of  the  heart's  action  ;  and  (to  a  much  less 
extent)  {c)  the  condition  of  the  arterial  coats.  In  the  normal 
condition  of  things  the  blood  takes  some  time  to  flow  from  the 
arterial  system  into  the  capillaries,  the  recoil  of  the  arteries  is 
gradual,  and  the  line  of  descent  is  sloping. 

When  the  outflow  from  the  arterial  system  is  more  difficult 
than  in  health,  as  for  example,  in  the  cirrhotic  form  of  Bright's 
disease,  the  line  of  descent  is  still  more  gradual.  Vice  versd 
when  the  outflow  from  the  arterial  system  is  very  rapid  in 
consequence  of  a  dilated  condition  of  the  small  arteries  and 
capillaries;  and  in  aortic  regurgitation,  in  which  the  arteries 
suddenly  collapse  in  consequence  of  the  back  flow  through 
the  aortic  valves,  the  line  of  descent  becomes  more  and  more 
vertical  in  proportion  to  the  freeness  of  the  outflow  and  the 
rapidity  of  the  action  of  the  heart. 

The  dicrotic  wave,  or  the  aortic  systolic  ivave,  as  it  may 
be  called,  is  usually  present  in  a  normal  pulse  tracing,  and 

'  The  line  of  descent  is  sloping,  because  the  recoil  of  the  artery  is  gradual.  In 
this  respect  there  is,  therefore,  a  marked  difference  between  the  up-stroke  and  the 
line  of  descent 


252  Diseases  of  the  Heart. 

corresponds  to  that  period  of  the  cardiac  cycle  which  imme- 
diately follows  the  closure  of  the  aortic  valve  cusps  :  while 
the  point  of  the  tracing  which  immediately  precedes  it  {e  in 
fig.  78),  and  which  is  generally,  but  not  universally,^  believed 
to  correspond  in  time  to  the  closure  of  the  aortic  segments, 
is  termed  the  aortic  notch. 

Where  the  vaso-motor  tone  is  very  good,  and  the  arterial 
tension  high,— as  it  is  in  some  healthy  persons, — the  dicrotic 
wave  is  very  feebly  marked  or  altogether  absent.  (See 
fig.  ^l) 


Fig.    83. — Pulse  fracinq;  of  good  tension  (/pressure  3  oz. )     The  pulse  is  slightly 
irregular,  but  otherwise  normal  ;  the  dicrotic  wave  is  scarcely  perceptible. 

The  exact  cause  of  the  dicrotic  wave  has  given  rise  to  much  debate  ; 
but  most  physiologists  are  agreed  that  it  is  in  great  part  due  to  the 
recoil  current  from  the  closed  aortic  valve, — an  opinion  which  is  con- 
firmed by  cHnical  observation.  Dr  Galabin,  while  agreeing  that  the 
great  cause  of  the  dicrotic  wave  is  a  recoil  current  from  the  aortic 
valves,  thinks  that  its  production  is  aided  by  the  inertia  of  the  fluid. - 

Dr  Roy  differs  from  this  opinion.  As  the  result  of  careful  experiment, 
he  suggests  that  the  secondar)'  waves  which  appear  in  the  unopened 
artery  under  normal  blood-pressure,  are  the  result  of  an  active  vemii- 
cular  contraction  of  the  muscular  coat  of  the  arteries.  He  completely 
rejects  the  theories  which  would  ascribe  these  undulations  to  reflected, 

'  A  TVx/ y9^(7.^^/'/2)'J/o/c^l',  4th  edition,  by  Professor  Michael   Foster,  p.  172. 

*  Dr  Galabin  explains  the  mode  of  production  of  the  dicrotic  wave  in  the 
following  manner  : — '  The  first  cause  of  the  dicrotic  wave  is  that  which  has  been 
very  generally  accepted  as  depending  upon  the  aortic  valves.  For  let  us  con- 
sider a  section  of  artery  close  to  the  valves.  When  the  influx  from  the  heart 
suddenly  ceases  at  the  end  of  systole,  the  fluid  for  an  instant  continues  to  flow 
away  out  of  the  section  on  account  of  its  acquired  velocity,  and  the  pressure  in 
the  section,  therefore,  rapidly  falls,  and  the  artery  contracts.  As  soon  as  the 
velocity  of  the  fluid  is  checked  bythe  pressure  in  front,  a  reflux  takes  place,  which, 
being  stopped  by  the  valves,  causes  a  second  increase  of  pressure  and  second 
expansion.  This  is  propagated  as  the  dicrotic  wave  into  the  periphery,  and  may 
itself  again  call  out  a  second  similar  oscillation  or  tricrotic  wave,  which  is  not 
unfrequently  seen  in  the  pulse.  Even  in  the  total  absence  of  aortic  valves,  the 
reflux,   meeting  with    the    current    entering    the    ventricle,   may  cause  a  second 


Analysis  of  a  Sphygmjgrapliic  Tracing.         253 

opening  and  closing  waves,  etc.,  or  in  fact  to  secondary'  waves  at  all,  of 
whatever  character.  The  tracings  which  he  obtained  from  the  opened 
arter)'  of  a  rabbit,  under  a  normal  blood-pressure,  never  showed  'the 
slightest  trace  of  secondary  waves  superposed  on  the  primary'  or  pulse 
wave,'  although  the  instrument  he  used  was  quite  delicate  enough  to 
record  them  did  they  really  exist.' — Michael  Foster's  Journal  of  Phy- 
siology, 1879-80,  p.  76. 

The    dicrotic   wave   is   absent    or   feebly    marked    in   free 
aortic  regurgitation.     (See  figs.  84  and  85.) 


Fig.  84. — Pressure  -i\  oz.  Fig.  85. — Pressure  3  oz. 

Fig.  84. — Aortic  Regurgitation. — Case:  G.  A.,  jet.  56,  admitted  to  Newcastle 
Infirmar}'  21st  February  1878,  suffering  from  shortness  of  breath  and  swell- 
ing of  feet.  Had  been  iU  for  three  months.  The  face  was  pale  and  anxious, 
lips  slightly  dusky.  Double  aortic  murmur ;  heart  considerably  h}-per- 
trophied  ;  apex  beat  between  6th  and  7th  ribs,  3  inches  below  and  2  inches 
outside  left  nipple.  Considerable  hypertrophy  and  engorgement  of  right 
heart.  Died  5th  March  1878.  Aorta  very  atheromatous  ;  aortic  valves 
very  incompetent  ;  segments  shrunken,  turned  in  towards  the  ventricle  ; 
coronary  arteries  much  obstructed  ;  cardiac  walls  fatty  ;  left  ventricle  dilat- 
ed ;  pericardium  adherent.  The  arteries  were  practically  empty  during  the 
ventricular  diastole.  a-^=up-stroke  ;  (J=apex  ;  <-=  tidal  wave  ;  t/ indicates 
the  position  of  the  aortic  wave,  which  is  absent  in  this  tracing. 

Fig.  85. — Aortic  Regurgitation. — Taken  from  the  same  patient  as  No.  84,  after  ad- 
ministration of  digitalis.    The  letters  have  the  same  significance  as  in  fig.  84. 

increase  of  pressure  or  dicrotic  wave,  although  this  will  be  much  less  than  in  the 
former  case.  If  the  fluid  in  the  tubes  be  air  instead  of  blood  or  water,  its  mo- 
mentum is  so  small  that  its  velocity  is  checked  instantly  at  the  end  of  systole, 
and  there  is  no  perceptible  dicrotic  wave.  If,  on  the  contrary,  mercurj'  be  taken, 
both  the  dicrotic  and  succeeding  waves  become  enormous,  on  account  of  the  great 
momentum  of  the  fluid,  as  was  shown  by  Marey.  The  fluid  remaining  the  same, 
the  oscillation  will  be  more  ample  the  greater  the  initial  velocity,  and  the  more 
slowly  that  velocity  is  checked.  Thus  dicrotism  is  promoted  by  a  sudden  action 
of  the  heart,  and  also  by  distensibility  of  arteries,  by  lowness  of  arterial  pressure, 
and  by  freedom  of  outflow.  I  think  that  in  considering  this  origin  of  the  dicrotic 
wave,  sufficient  attention  has  not  generally  been  paid  to  the  important  part  played 
in  it  by  the  inertia  of  the  fluid,  and  to  the  fact  that  the  aortic  valves,  although 
extremely  important,  are  not  absolutely  essential.' — Journal  of  Anatomy  and 
Physiolog)',  vol.  x.  p.  303. 


2  54  Diseases  of  the  Heart. 

It  is  also  faintlv  marked  in  some  pulses  of  high  tension, 
and  in  some  cases  in  which  the  elasticity  of  the  arteries  is 
much  impaired,  as  in  advanced  atheroma. 

It  is  sometimes  greatly  exaggerated,  and  the  pulse  is 
then  said  to  be  dicrotic  (see  figs.  87,  88,  and  89). 


Pressure  3  oz. 

P'lG.  87. — Dicrotism. — A.  H.,  a?t.  32,  admitted  to  Newcastle  Infirmary  21st 
March  1878,  with  an  enormous  scrofulous  kidney.  There  were  occasional 
rigors.     This  tracing  was  made  during  a  rigor,  the  temperature  being  100°  F. 


Fig.  88. — Irregular  and  Dicrotic  Pulse  in  Pneumonia. — ^J.  R.,  set.  68,  admitted  to 
the  Newcastle  Infirmary  28th  December  1878.  Died  31st  December.  Croupous 
pneumonia,  limited  to  the  upper  lobe  of  the  right  lung.     No  cardiac  affection. 


Fig.   89. — Dicrotic  Pulse  from  a  case  of  Rheumatic  Fever. 

Degrees  of  dicrotisvi,  and  t/ieir  significance.  —  Various 
degrees  of  dicrotism  occur,  'to  which  terms  have  been  ap- 
plied indicating  the  relation  of  what  is  known  as  the  "  dicrotic 
notch"  to  the  respiratory  line  of  the  tracing'   (Mahomed).^ 

'   Cantos  .Surgery,  vol.  i.  p.  56. 


The  Dicrotic  JFave. 


255 


They  may  be  said  to  represent  the  relative  condition  of  the 
artery  at  the  point  where  the  sphygmograph  is  appHed,  as 
regards  its  fulness  or  state  of  distention  at  the  commence- 
ment, and  at  the  termination  of  the  ventricular  systole  re- 
spectively. 

(a)  When  the  dicrotic  wave  is  well  marked,  but  the  aortic 
notch  C  is  above  the  base  line  A  B  (see  fig.  90),  the  pulse 
is  called  dicrotic.  In  this  condition  the  artery  is  more  dis- 
tended at  the  end  of  the  ventricular  systole  than  it  is  at  the 
commencement. 


Fig.  90. — Dicrotic  Pulse.     ( After  MaJiomed. )    A  B,=base  line  ;  C,  =  aortic  notch. 


Fig.   91. — Fully  Dicrotic  Pulse.     (After  Mahomed.)      A  B,=base  line; 
C,=  aortic  notch. 

(^)  When  the  .aortic  notch  C  reaches  the  level  of  the 
respiratory  or  base  line  A  B,  the  pulse  is  called  y>///^'  dicrotic. 
In  this  condition  the  artery  is  apparently  no  more  distended 
at  the  end  of  the  ventricular  systole  than  it  is  at  its  com- 
mencement, and  it  is  apparently  less  distended  than  it  is 
during  the  ventricular  diastole^  (see  fig.  91). 

(c)  When  the  aortic  notch  C  sinks  below  the  level  of  the 

'  This  does  not  of  course  imply  that  the  arterial  system,  as  a  whole,  is  more 
empty  at  the  end  of  the  ventricular  systole  than  it  is  during  the  ventricular 
diastole,  but  simply  that  the  vessel  at  the  point  where  the  observation  is  taken, 
apparently  presents  such  a  condition  ;  I  say  apparently,  for  the  depression  of  the 
curve  at  the  end  of  the  ventricular  systole  is  doubtless  in  part  due  to  the  sudden 
fall  of  the  lever  itself 


256  Diseases  of  t lie  Heart. 

respiratory  line  A  B,  the  pulse  is  called  Jiyperdicrotic.  (See 
fig.  92).  In  this  condition  the  artery  (at  the  point  of  obser- 
vation) is  appare7itly  less  distended  at  the  termination  of  the 
ventricular  systole  than  it  is  at  its  commencement. 


Fig.  92 — HyperJkrotic  Pulse.     { After  Malioiiied.  )     A  B,  =  base  line  ;  C,=aortic 

notch. 

When  dicrotism  is  well  marked,  i.e.,  when  the  pulse  is 
fully  dicrotic,  each  cardiac  cycle  is  (apparently)  attended  by 
two  pulse  beats,  hence  the  term  dicrotic,  or  double  pulse. 

Tlic  conditions  ivhich  favour  dicrotism  arc : — 

1.  A  low  condition  of  arterial  tension. 

2.  Freedom  of  outflow  from  the  arterial  system,  i.e. 
through  the  capillaries. 

(Both  of  these  conditions  are  usually  due  to  one  and  the 
same  cause,  viz.,  loss  of  vaso-motor  tone). 

3.  A  sudden  sharp  ventricular  systole. 

4.  Elasticity  of  the  arterial  walls. 

According  to  Dr  Burdon  Sanderson,  'dicrotism  is  cha- 
racteristic of  that  condition  of  the  circulation  in  which  the 
arterial  pressure  is  diminished,  while  the  venous  is  increased. 
It  denotes  that  the  capillary  current,  instead  of  being  con- 
stant in  its  rate  of  movement,  is  markedly  accelerated  during 
diastole,  and  retarded  during  the  diastolic  interval.' 

Dr  Roy  thinks  that  the  dicrotic  wave  of  fever,  which  is 
associated  with  reduced  blood-pressure,  is  due  to  a  secondary 
and,  most  probably,  reflected  wave. 

He   found  that  any  considerable    reduction  of  the    medium   blood- 
pressure,  from  whatever  cause,  leads    to    the    appearance  of  a  dicrotic 
pulse-wave    in    tracings    both    from    the  opened    and    unopened    arter^^ 
This  form  of  dicrotism,'  he  savs,  'must  not  be  confounded,  as  is  often 


Causes  of  Dicrotisin.  257 

done,  with  those  undulations  more  or  less  marked,  which  gave  to  the 
pulse  curve  in  health  its  characteristic  outline.  The  dicrotism  from  re- 
duction of  blood-pressure,  as  it  is  seen  in  tracings  from  the  now  opened 
arteiy,  is  characterised  by  the  fact,  that  it  does  not  disappear  when  the 
extra-arterial  pressure  is  raised  nearly  as  high  as  the  blood-pressure, 
showing  that  it  is  really  due  to  a  secondary  and  most  probably  reflected 
wave.' — Micliacl  Foste7''s  yoiirnal  of  Plivsiology,  1S79,  1880,  p.  80. 

Clinically,  the  pulse  is  dicrotic  in  cases  in  which  the 
nerve  tone  (vaso-motor  system)  is  feeble.  Many  persons 
who  apparently  enjoy  good  health  have  dicrotic  pulses 
Such  persons  are  easily  'knocked  up,'  are  unable  to  undergo 
any  severe  and  prolonged  strain,  and  are  most  unfavourable 
subjects  for  an  attack  of  continued  fever  ;  in  them  a  severe 
pneumonia,  or  an  attack  of  typhus,  would  almost  certainly 
be  fatal.  A  comparatively  slight  elevation  of  temperature  in 
such  persons  causes  the  pulse  to  become  />///)'  dicrotic  or  even 
hypcrdicrotic.     (See  figs.  93,  94,  95.) 


Fig.  93. — Pressure  3  oz.         Fig.  94. — Pressitre  3  oz.         Fig.  95. — Pressure  4  oz. 

Fig.  93. — Dicrotism. — A.  H.,  £et.  32,  admitted  to  Newcastle  Infirmary  21st 
March  1878,  with  an  enormous  scrofulous  kidney.  There  were  occasional 
rigors.  This  tracing  was  made  during  a  rigor,  the  temperature  being 
100"  F.  A  draught  of  hot  milk  was  administered,  and  the  tracing,  shown  in 
fig.  94,  was  taken.     Tracing  fig.  95  a  few  minutes  later. 

Fig.  94. — HyperdicrotisDi.  Fig.  95.  —Hyperdicrotism. 

The  great  clinical  condition  with  which  dicrotism  is 
associated  is  pyrexia.  Where  a  considerable  elevation  of 
temperature  (I02°-I04°  Fahr.)  continues  for  some  time,  as  in 
enteric  and  typhus  fever  for  example,  the  pulse  usually 
becomes  dicrotic.  A  dicrotic  pulse  under  such  circumstances 
indicates  the  free  administration  of  stimulants. 

Hypcrdicrotism  is  (as  a  rule)  only  seen  in  cases  of  high 
fever  with  great  exhaustion,  but  in  debilitated  subjects  it 
may,  as   I   have  previously   remarked,  be  produced  by  slight 

R 


2^^  Diseases  of  the  Heart. 

elevations  of  temperature.  In  the  hyperdicrotic  pulse  the 
second  (dicrotic)  beat  is  cut  short  by  the  up-stroke  of  the 
ventricular  systole  of  the  next  beat. 

If  the  rapidity  of  the  hyperdicrotic  pulse  is  increased  the 
second  beat  is  lost  altogether,  and  the  pulse  is  then  said  to 
be  mojwcrotic.     (See  fig.  96.) 


Fig.  96. — Monocrotic  Pulse.     (After  Riegel.) 

The  prcdicrotic,  true  tidal,  or  second  ventricular  systolic 
wave. 

Between  the  apex  of  the  tracing  and  the  aortic  notch  a 
second  wave  (see  fig.  78)  is  often,  but  not  always,  seen,  Dr 
Mahomed  thinks  that  it  corresponds  to  the  steady  onward 
passage  of  the  blood  which  results  from  the  ventricular  systole, 
hence  he  has  termed  it  the  true  tidal  wave.  It  is  sometimes 
called  the  predicrotic  w'dLWQ,  because  of  its  relationship  to  the 
dicrotic  wave.  It  may,  I  think,  with  advantage  be  termed 
the  second  ventricular  systolic  wave,  for  it  occurs  after  the 
apex  or  first  ventricular  systolic  wave,  and  during  the  systole 
of  the  ventricle. 

The  essential  condition,  which  favours  the  production  of 
the  second  ventricular  systolic  wave,  is  increase  of  the  arterial 
tension  during  the  ventricular  systole.  This  condition  (in- 
creased arterial  tension)  is  usually  due  to  difficulty  of  arterial 
outflow  as  in  Bright's  disease  (see  figs.  97  and  98),  and  in 
atheroma  (see  fig.  99);  but  it  may  also  result  from  an  excessive 
amount  of  blood  being  propelled  into  the  arterial  system  at 
each  ventricular  systole.  An  excellent  clinical  example  of 
the  latter  condition  is  seen  in  aortic  regurgitation,  in  which  a 
powerful  and  dilated  ventricle  propels  a  large  quantity  of 
blood  into  the  arterial  system,  producing  high  tension  during 
systole,  with  a  well-marked  predicrotic  luave,  but  in  which  the 


The  Predicrotic  Wave.  259 

arterial  pressure  during  the  ventricular  diastole  is  extremely 
feeble.^ 


J'l-t'ssiirc  3  oz.  Pressure  4  oz. 

F'lo.   97.  —  Chronic   Brighfs   Disease.  —  I),    (.i.,   s-t.    40,    admitted    to   Newcastle 

Infirmary  5th  September   1878,  sutit'ering  from  renal  dropsy   (large  white 

kidney).     The  pulse  is  one  of  high   tension  ;    the  tidal   wave  is  strongly 

marked. 
Fin.   98. — Acute  Bright' s  Disease. — Tidal  wave  strongly  marked,  from  a  patient 

admitted  to  the  Newcastle  Infirmarv  under  the  care  of  Dr  Drummoncl. 


Fig.  99. — Atheroma  and  Aneurism  of  Aortic  Arcli. — J.  D.,  set.  52,  admitted  to 
Newcastle  Infirmary  2lst  February  1878,  suffering  from  aneurism  of  the 
ascending  portion  of  the  aortic  arch  and  atheroma.  The  tidal  wave  is  very 
strongly  marked.  There  was  no  perceptible  difference  between  the  two 
pulses. 

Vice  versa  the  second  ventricular  systolic  wave  is 
absent  in  those  cases  in  which  the  arterial  tension  during 
the  ventricular  systole  is  low.  Now,  low  tension  during  the 
ventricular  systole  may  be  due  either  to  an  insufficient 
amount  of  blood  being  pumped  into  the  arterial  system 
during  the  ventricular  contraction,  a  condition  which  is  seen 
in  cases  of  cardiac  weakness,  mitral  disease,  etc.  ;  or,  it  may 
result  from  an  abnormally  free  outflow  from  the  arterial 
system  during  the  ventricular  systole,  a  condition  which  is 

'  Dr  Galabin  (forrtierly)  supposed  that  the  separation  of  the  primary,  or  so 
called  '  percussion '  and  tidal  waves  did  not  really  exist  in  the  artery,  but  was 
produced  in  the  trace  by  the  velocity  acquired  by  the  sphygmograph  in  the 
sudden  primary  up-stroke.  Further  observation,  Restates,  'has  convinced  him 
that,  although  this  explanation  applies  to  many  cases,  it  yet  does  not  express  the 
whole  truth,  and  that  in  some  instances  at  least  there  is  a  real  first  secondary 
wave  or  oscillatory  expansion  in  the  artery,  i.e.  the  tidal  or  predicrotic  wave.' — 
yournal  of  Anatomy  and  Physiology,  vol.  x.  p.  299. 


26o 


Diseases  of  the  Heart. 


due  to  a  dilated  condition  of  the  small  arteries  and  (?)  capil- 
laries. In  such  cases  the  pulse  rapidl}'  falls  a\va\'  during  the 
ventricular  systole,  in  other  words,  after  the  first  distention  of 
the  arterial  wall  there  is  a  quick  and  rapid  collapse,  which  is 
only  arrested  by  the  occurrence  of  the  dicrotic  wave;  and  this 
is,  as  we  have  seen,  chiefly  a  recoil  wave  from  the  closed  aortic 
valves.  A  rapid  collapse  of  this  description  is  best  marked 
in  the  dicrotic  and  hyperdicrotic  pulse  of  fever,  and  in  con- 
ditions of  vaso-motor  debility  and  relaxed  vessels.  Hence 
it  will  be  easily  understood  why  in  these  cases  the  second 
ventricular  systolic  wave  is  not  present. 


h  IG.    \oo.— Irregular  Fiilse  in  mitral  regurgitation,  with  hypertrophy  of  the  Left 
Ventricle. — In  the  tallest  curves  the  tidal  wave,  a,  is  well-marked,  while  it 

is  absent  in  the  smaller  ones.    The  letters  <^7.  a.  point  to  the  predicrotic  wave. 


Pressure  4^  oz. 
Fig.    ioi.  —  General  Atheroma. — J.  U.,  a?t.   60,  admitted  to  Newcastle   Infirmary 
2 1  St  October   1878.     The  radials  were  very  tortuous  and  rigid  ;  there  was 
no  valvular  lesion.     The  tidal  wave  only  occurs  every  alternate  beat. 

It  not  untVequently  happens  that  the  predicrotic  wave 
is  present  in  some  pulse  curves  of  a  tracing,  but  absent  in 
others.  This  condition,  which  depends  of  course  upon  the 
fact  that  the  arterial  pressure  during  the  ventricular  systole 
is  greater  during  some  pulsations  than  during  others,  is 
especially  frequent  in  mitral  stenosis,  in  which  condition  a 
varying  amount  of  blood  is  apt  to  be  discharged  into  the 
cavity  of  the  left  ventricle,  and  thence  into  the  arterial  system. 
(See  fig.  100.)  Occasionally  the  predicrotic  wave  occurs  every 
alternate  beat,  as  show^n  in  fig.  loi  ;  in  that  case  the  irregu- 
larity was  probably  due  to  nervous  causes. 


The  Predicrotic  W'az'c.  261 

Other  secondary  waves  sometimes  occur  in  the  lower  part 
of  the  Hne  of  descent.  Their  exact  cause  is  obscure,  but 
so  far  as  is  at  present  known,  they  are  of  little  practical 
importance. 

These  waves  are  probably  as  a  rule  due  to  the  inertia  of  the  instru- 
ment. Occasionally  a  small  wave  is  seen  to  occur  immediately  before 
the  up-stroke,  i.e.  immediateh'  before  the  contraction  of  the  ventricle. 
Possibly  it  may  be  due  to  the  contraction  of  the  left  auricle. 

Respiratory  or  base  li)u\ — In  a  normal  tracing  the  lowest 
points  of  the  up-strokes  of  succeeding  pulse  waves  are  on  the 
same  horizontal  plane  (see  hg.  "'i),  and  a  line  drawn  through 
the  bases  of  the  up-strokes  is  called  the  base  or  respiratory 
line.  The  latter  term  (respiratory  line)  is  applied  to  the  base 
line  because  inspiration  and  expiration  exert,  sometimes  even 
in  health,  but  notably  in  some  cases  of  disease,  a  marked 
influence  upon  it.  During  a  full  and  sudden  inspiration  the 
arterial  tension  is  lowered,  and  the  base  line  falls  ;  during 
expiration,  on  the  contrary,  the  arterial  tension  is  increased, 
and  the  base  line  rises.  In  cases  of  spasmodic  asthma  and 
severe  dx'spncea  the  base  line  max*  be  very  uneven.  (See 
figs.  lOi,  102.) 


Preisiirc  3I  01. 
Fig.    102.  —  Uneven    Respiratory    Line. — |.     K.,   itt.    31,    adniittecl   to   Newcastle 
Infirmary  26th  December  187S,  sufterinc;  from  acute  bronchitis. 


Fig.    103.  —  Uneven  Respiratory  Line  (from  a  ease  of  Spasiiiodie  Astliina). 
The  tracing  was  taken  during  the  paroxysm. 


262  Diseases  of  the  Heart. 

In  the  normal  pulse-tracing,  during  ordinary  (tranquil) 
respiration,  each  consecutiv'^e  pulse  curve  is  an  exact  repeti- 
tion of  the  preceding  one;  in  other  words,  the  pulse  is  regular 
in  time,  the  different  pulse  waves  are  equal  in  volume,  and 
the  individual  character  of  succeeding  pulse  curves,  in  respect 
to  the  different  parts  of  which  they  are  composed,  is  the 
same.  When  the  pulse-tension  is  low,  or  when  the  respiration 
is  active,  succeeding  pulse  curves  are  seldom  quite  identical, 
but  are  more  or  less  modified  by  inspiration  and  expiration, 
as  described  above. 

Having  analysed  the  normal  pulse  tracing,  and  described 
the  more  important  modifications  which  it  undergoes,  I  will 
next  proceed  to  consider  the  character  of  the  pulse  in  health 
and  disease. 

THE   FREQUENCY   OF   TME   PULSE. 

The  frequency  of  the  pulse  is  determined  by  counting  the 
number  of  pulsations  which  occur  in  a  minute.  To  insure 
accuracy,  the  pulse  should  be  counted  for  a  whole  minute, 
and  not  for  a  quarter  of  a  minute,  as  is  sometimes  done.  In 
some  cases  in  which  the  pulse  at  the  wrist  is  very  feeble, 
the  frequency  of  the  cardiac  contractions  can  be  best  deter- 
mined by  auscultation  over  the  praecordia. 

The  exact  frequency  of  the  pulse  can  also  be  determined  by  means 
of  the  sphygniograpb.  Mahomed's  modification  of  Marey's  instrument 
is  so  constructed  that  four  inches  of  the  shde  are  propelled  past  the 
point  of  the  writing  lever  in  ten  seconds.  In  order,  therefore,  to  ascer- 
tain the  frequency  of  the  pulse  per  minute,  the  number  of  pulse  waves  in 
four  inches  of  the  tracing  must  be  multiplied  by  six.  Dudgeon's  instru- 
ment is  also  constructed,  so  that  six  times  the  number  of  pulsations, 
traced  on  the  slip  of  paper,  give  the  number  of  beats  per  minute.' 

In  counting  a  veiy  rapid  pulse,  Dr  Abbot  describes,  in  the  Neiu  York 
Medical  Record  for  August  12,  1882  (quoted  in  the  Medical  Times  and 
Gazette.,  September  30,  1882),  a  method  which  he  adopted  for  counting 
the  heart's  action  during  some  experiments  he  performed  with  alcohol 
on  birds.       He  found  that  he  was  unable  to  count  by  the  usual  mode 

'  These  measurements  only  hold  good  so  long  as  the  slide  is  travelling  at  full 
speed.  To  insure  accuracy,  therefore,  the  clock-work  should  be  fully  wound  up 
before  the  tracing  is  taken. 


The  Frequency  of  the  Pulse.  26 


v) 


when  the  cardiac  contractions  exceeded  240  per  minute,  whereas,  by  the 
method  he  now  describes,  he  easily  counted  280.  '  During  a  definite 
part  of  a  minute,  usually  one-fourth,  dots  were  made  with  a  lead  pencil 
upon  a  sheet  of  paper,  syitchronous  with  the  hearfs  beats,  as  heard  over 
the  cardiac  region.  The  dots  were  then  counted.  A  pulse  oi  four 
hundred  could  be  taken  in  this  way,  provided  each  pulsation  were 
distinct  enough  to  be  discriminated  by  the  touch.  The  indistinctness  of 
the  separate  pulsations  alone  fixes  the  limits  to  the  use  of  this  method, 
as  the  human  Jiand  is  capable  of  making  intelligently  and  with  accuracy 
at  the  rate  of  450  dots  per  minute,  for  thirty  seconds,  which  rate  is 
probably  beyond  not  only  that  of  the  human  heart,  but  also  of  the  pulse 
of  any  of  the  lower  animals  available  for  experiment.  I  have  had  a 
sufficient  experience  with  this  method,'  he  says,  'to  know  that  it  is  of 
practical  value,  especially  with  children.  All  movements,  whether  of  the 
body  or  not,  that  can  be  seen,  felt,  or  heard,  can  be  thus  counted  up 
to  400  or  500  per  minute,  provided  that  they  are  sufificiently  distinct  to 
be  discriminated.' 

Frequency  in  health. — The  normal  frequency  varies  in  dif- 
ferent individuals,  and  in  the  same  individual  under  different 
circumstances.  The  average  normal  rate  in  the  adult  male 
in  a  state  of  rest  is  72,  but  there  are  many  exceptions.  In 
some  persons  the  pulse  rate  is  habitually  as  high  as  100,  in 
others  as  low  as  50.  In  practice,  therefore,  such  idiosyncracies 
must  be  kept  in  view.  The  pulse  is  quicker  in  children  than 
in  adults,  but  it  quickens  slightly  again  in  old  age  ;  it  is 
quicker  in  women  than  in  men.  The  pulse  rate  is  increased 
by  active  exercise  (bodily  or  mental).  It  varies,  too,  with 
the  position  of  the  body,  being  quicker  in  the  standing  than 
in  the  sitting,  and  in  the  sitting  than  in  the  recumbent  posi- 
tion. Its  frequency  also  varies  with  the  time  of  day,  being 
lower  in  the  early  morning  hours.  It  is  decreased  during 
sleep  and  increased  after  a  meal.  It  varies  with  the  tempera- 
ture of  the  body,  and  is  to  a  slight  extent  influenced  by  the 
atmospheric  pressure.  The  frequency  of  the  pulse  is  also 
profoundly  influenced  by  emotional  disturbances,  and  by  the 
mental  condition,  hence  it  is  often  difficult  to  get  a  proper 
estimate  of  the  pulse-rate  in  children  and  nervous  persons, 
the  mere  presence  of  the  doctor  being  sufficient  to  increase 
the  frequency  by  10,  20,  30,  or  even  40  beats.  Due  allow- 
ance must  of  course  be  made  for  this  and  other  disturbing- 


264 


Diseases  of  tJic  Heart. 


causes.  It  is  often  a  good  plan  to  count  the  pulse  at  the 
end  of  the  visit,  or  at  all  events  to  allow  sufficient  time 
for  any  temporar\'  alteration  in  the  pulse-rate  to  have  dis- 
appeared. 

TABLE  OF  THE  AVERAGE  PULSE  RATE  AT  DIFFERENT  AGES. 


Foetus  in  utero, 
Child  newly  born, 
1st  year, 
„  2d  year, 

„         3d  year, 
7th — 14th  year. 
14th — 20th  year, 
2 1  St — 60th  year, 
Old  age, 


about  140 
140—135 

120 — 1 10 
105 — 100 
100 —  85 
85—  80 
80—  72 
70—  75 
75-  80 


Alterations  in  the  pulse-rate,  ivJiicli  oceiir  in  disease. 

The  pulse-rate  may  be  either  increased  or  diminished  by 
disease. 

The  pulse-rate  is  increased  in  : — 

I.  Pyrexia  (increased  temperature). — As  a  general  rule 
the  amount  of  increase  varies  with  the  height  of  the  tem- 
perature. According  to  Dr  Aitken,  an  increase  of  tem- 
perature of  one  degree  above  98°  Fahr.  corresponds  with 
an  increase  of  ten  beats  of  the  pulse  per  minute,  as  shown 
in  the  following  table  : — 


Temp.  Fahr. 

Pulse-rate. 

Temp.  Fahr. 

Pl 

Ise-rate 

98° 

60 

103° 

I  10 

99° 

70 

104° 

120 

100° 

80 

105° 

130 

101° 

90 

106° 

140 

102° 

100 

Exceptions. — In  some  cases  of  typhoid,  especially  in  its 
earlier  stages,  and  in  meningitis,  the  pulse  may  be  slower 
than  natural.  At  the  commencement,  too,  of  some  cases  of 
pericarditis  the  frequency  of  the  pulse  is  diminished — (Stokes). 

2.  Conditions  associated  zuit/i  extreme  debility.— This  is 
chiefly  the  case  where  there  has  been  some  previous  elevation 
of  temperature,  or  where  the  nerve  irritability  of  the  heart 
is  increased. 


Increased  Frequency  of  the  Pulse.  265 

3.  Cases  in  ivhich  the  vagus  is  paralysed  or  the  cervical 
sympathetic  irritated — In  these  cases  the  nerve  balance  of 
the  heart  is  deranged,  and  the  pulse-rate  increased.  In  a 
few  cases  (as  for  instance,  in  exophthalmic  goitre  in  which  the 
sympathetic  is  irritated,  and  in  the  later  stages  of  basilar 
meningitis,  in  whicli  there  is  probably  paralysis  ot  the  vagus), 
the  nerve  derangement  depends  upon  organic  disease  ;  but 
in  the  large  majority  of  cases,  as  in  hysteria,  in  which  affec- 
tion the  pulse  frequency  may  be  enormousl)'  increased,  the 
condition  is  a  functional  one. 

4.  Some  cases  of  organic  cardiac  disease,  especially  mitral 
regurgitation  (see  fig.  104),  and  (to  a  less  extent)  in  aortic 
regurgitation  (see  fig.  105). 


Pressure  3  oz. 

Fig.  104. — Mitral  RegurgUat ion. — M.  A.  C,  aet.  16,  admitted  to  Newcastle  In- 
firmary 24th  January  1878,  suffering  from  cough  and  shortness  of  breath, 
dating  from  an  attack  of  rheumatic  fever  two  months  previously.  Heart's 
action  very  rapid  (120-130).  The  first  sound  appeared  to  be  reduplicated  ; 
a  systolic  murmur  was  audible  at  the  apex  when  the  heart  became  slower. 


Fig.    105. — Pulse  tracing  from  a  Case  of  Aortic  Regurgitation  ^ 

The  Clinical  Significance  of  Increased  Frequency  of  the  Pulse, 

Increased  frequency  of  the  pulse,  when  not  merely  tem- 
porary, is  very  suggestive  of  pyrexia  ;  it  is,  however,  per  se, 
an  unreliable  sign  of  fever,  for,  on  the  one  hand,  fever  may  be 
present  without  any  increase  (a  diminished  pulse-rate  being, 
as  I  have  already  pointed  out,  sometimes  met  with,  as  in  the 
earlier  stages  of  typhoid  and  in  meningitis) ;  and,  on  the 
other,  increased  frequency  of  the  pulse   may  occur  without 


2  66  Diseases  of  the  Heart. 

fever,  or  even  with  a  low  temperature,  as  in  pro-agonistic 
collapse.  In  order  to  ascertain  the  cause  of  the  increased 
frequency  of  the  pulse,  the  first  step  is  to  take  the  tempera- 
ture. If  there  is  no  pyrexia,  the  causes  mentioned  under 
heads  2,  3,  4  must  be  looked  for. 

A  slow  pulse  may  be  due  to — 

1.  Functional  derangement  of  the  heart. — This  is  pro- 
bably the  cause  of  the  slow  pulse  which  occurs  in  jaundice, 
in  some  cases  of  gout,  etc. 

Non-febrile  jaundice  usually  produces  a  retarded  action  of  the  heart 
and  diminished  arterial  tension.  The  pulse  may  fall  to  50,  40,  or  even 
20  beats  in  the  minute,  and  it  may  also  be  irregular. 

Dr  Wickham  Legg  and  others  believe,  that  the  slowness  of  the  pulse 
is  produced  by  the  presence  of  unchanged  biliaiy  acids  in  the  blood. 

Dr  Murchison  has  seen  a  slow  pulse  (36-60  per  minute)  in  cases  of 
hepatic  disease  in  which  there  was  no  jaundice. 

2.  Organic  lesions  of  the  heart,  such  as  fatty  degenera- 
tion of  the  left  ventricle  and  aortic  stenosis.  In  the  former 
case  (weakness  of  the  ventricular  wall)  a  slow  pulse  is 
perhaps  exceptional,  and  is  only  seen  when  the  patient  is 
at  rest.  Any  exertion  which  throws  a  strain  on  the  beat, 
is  attended  in  these  cases  with  a  quick,  rather  than  with 
a  slow,  pulse.  In  the  latter  case  (aortic  stenosis)  the  left 
ventricle  has  difficulty  in  emptying  itself,  its  contraction  is 
prolonged  and  somewhat  laboured,  and  the  frequency  of  the 
pulse  is  diminished. 

3.  Lesions  of  the  nervous  system,  in  which  the  cardio- 
inhibitory  centre  in  the  medulla  or  the  branches  of  the  vagus 
which  pass  from  that  centre  to  the  heart  are  irritated 
(stimulated).  In  some  cases  the  condition  is  a  temporary 
(functional)  one,  as  for  example,  in  those  cases  in  which  a 
slow  pulse  is  associated  with  a  neuralgic  headache  (megrim); 
in  others,  as  for  example  meningitis  (in  the  earlier  stages  of 
which  the  pulse  may  be  abnormally  slow),  the  lesion  is  organic. 

4.  The  rapid  defervescence  of  fever ;  the  pulse-rate  may 
in  these  cases  rapidly  fall  from  a  high  rate  to  a  point  much 
below  the  normal. 


DimmisJied  Frequency  of  the  Pulse.  267 

5.  Reflex  stimulation  of  the  cardio-iiiJiibitory  centre  in  the 
medtiUa. — The  reflex  impulse  may  in  all  probability  be 
generated  by  powerful  stimulatio*i  of  any  peripheral  nerve  ; 
but  it  most  frequently  arises  in  the  alimentary  tract. 

The  slow  pulse  which  is  so  frequently  seen  in  the  earlier  stages  of 
typhoid,  is  probably  due  to  reflex  inhibition  of  the  heart^the  local 
lesion  of  the  intestine  stimulates  the  mesenteric  nerves,  producing  an 
impulse  which  travels  to  the  medulla,  and  is  reflected  down  the  vagus 
to  the  heart. 

TJie  Clinical  Significance  of  a  Sloiv  Pulse. 

A  slow  pulse  per  sc  {i.e.  without  any  associated  signs  or 
symptoms)  is  of  little  practical  importance,  the  most  frequent 
cause  (provided  that  it  does  not  depend  upon  idiosyncracy) 
is  a  temporary  functional  derangement  of  the  heart.  The 
possibility  of  the  condition  being  due  to  irritation  of  the  vagi 
must  be  remembered,  and  the  symptoms  of  disease  at  the 
base  of  the  brain  or  in  the  course  of  the  vagus  looked  for. 
In  other  cases  {i.e.  where  there  are  associated  signs  and 
symptoms)  the  clinical  significance  of  a  slow  pulse  entirely 
depends  upon  the  cause  of  the  condition,  and  the  prognosis 
must  be  guided  accordingly. 

Variability  of  the  pulse-rate. 

The  pulse-rate  is  in  some  cases  liable  to  very  marked 
fluctuations.  In  the  convalescent  stage  of  fevers,  for  example, 
and  in  conditions  of  debility,  the  pulse-rate  is  very  variable  ; 
these  changes  are  readily  produced  by  any  trivial  movement 
or  mental  excitement.  I  have  noticed  the  same  liability 
to  rapid  changes  in  the  pulse-rate  in  the  earlier  stages  of 
some  cerebral  cases.  Extreme  variability  of  the  pulse-rate 
has  also  been  noticed  after  concussion  of  the  spine. ^ 

'  Dr  Guinoiseau,  quoted  in  the  Medical  Times  and  Gazette,  relates  in  the 
Bulletin  de  Th^rapeutiqiie,  February  28th  1882,  the  case  of  a  man  who  had 
received  a  concussion  of  the  spine  from  a  fall  from  a  carriage  on  May  9th,  1881. 
lie  recovered,  and  was  able  to  resume  his  occupation,  which  was  laborious; 
but  a  peculiarity  in  his  pulse  remained.  Examined  on  October  8th,  it  was 
found  that  his  pulse  was  49  when  recumbent,  73  when  seated,  and  109  when 
standing  ;  and  on  November  ist  the  pulse-rate  in  these  positions  was  respectively 
45.  57,  and  77. 


268 


Diseases  of  the  Heart. 


THE    RHVTH>[    OF   THE    PULSE. 

The  normal  pulse  (during  tranquil  respiration)  is  perfectly 
regular  (the  individual  pulse  waves  being  of  the  same  duration 
and  volume,  and  presenting  the  same  features  as  regards 
individual  curves)  ;  but  departures  from  the  normal  are  com- 
mon, indeed  in  some  persons  who  enjoy  perfect  health,  the 
pulse  is  habitually  irregular.  Such  idiosyncracies  are  more 
common  in  old  than  in  young  people. 

The  alterations  in  rliythvi  7u/iic/i  occur  in  disease  can  of 
course  be  observed  by  the  finger,  but  are  best  studied  by 
means  of  the  sphygmograph.  They  ma\-  consist  of  altera- 
tions in  time,  alterations  in  volume,  or  differences  in  the 
sphymographic  characters  of  the  individual  pulse  curves. 

Time  irregularities.  —  P\\\  degrees  of  time  irregularity  are 
met  with.  In  some,  the  alteration  is  only  occasional,  occurring 
every  ten,  twenty,  or  thirty  beats  ;  in  others,  the  normal 
rhythm  of  the  pulse  is  very  much  altered  or  entirely  lost. 
(See  fig.  io6.) 


Fir,,  106. — Extreme  iri-ei;ularity  of  the  pulse  from  a  Case  of  Pneumonia.  Five 
pulse  waves  are  shown  in  the  tracing,  which  was  taken  twenty-four  hours 
before  death. 


The  irregularity  sometimes  consists  in  the  omission  of  a 
beat  (see  figs.  107,  108)  ;  the  pulse  is  then  said  to  be  'inter- 
mittent.' Intermission  of  the  pulse  ma\'  be  due  either  to 
arrest  of  the  contraction  of  the  left  ventricle- a  condition 
which  is  not  uncommon  as  the  result  of  simple  nervous 
derangement,  and  is  then  of  comparatively  little  importance  ; 
or,  it  mav  be  owing  to  the  fact  that  some  of  the  ventricular 


The  R/iyt/uH  of  the  Pulse.  269 

contractions  fail  (are  too  feeble)  to  raise  the  aortic  valves  and 
send  into  the  arteries  a  pulse  wave  of  sufficient  strength  to 
be  felt  at  the  wrist. 


Fu;.    107. — Intermittent  Pulse. 


ssnre  4  oz. 

Fig.  108. — hiterniittent  Pulse. — J.  B.,  a?t.  38,  admitted  to  the  Newcastle  Infirmary 
nth  July  1878,  suffering  from  mitral  regurgitation.  The  heart  was  much 
hypertrophied.  Tracing  made  6th  January,  when  patient  was  much  im- 
proved and  attending  as  an  out-patient. 

This  latter  condition,  which  is  a  very  serious  indication 
of  heart-failure,  is  chiefly  met  with  in  those  cases  in  which 
the  heart-walls  are  degenerated  (dilatation,  fatty  and  fibroid 
degeneration),  but  is  also  seen  in  some  mitral  lesions. 

M  Marey,  quoted  by  Mahomed,  Gufs  tlospiial  Reports,  1879,  P-  397> 
gives  the  following  explanation  of  this  condition  : — '  In  a  heart  in  which 
mitral  regurgitation  occurs,  blood  is  forced  out  of  the  ventricle  in  two 
directions  during  systole  ;  one  portion  passes  through  the  aortic  orifice, 
the  other  is  driven  backward  into  the  auricle.  Now,  when  the  heart  is 
dilated,  it  sometimes  occurs  that  the  ventrical  contraction  is  not  of  suf- 
ticient  strength  to  overcome  the  arterial  resistance  and  raise  the  aortic 
valves  ;  it  finds  it  easier  to  force  all  the  blood  backwards  through  the 
incompetent  mitral,  which  thus  plays  the  part  of  a  safety  valve.  Meantime 
this  intermission,  which  is  caused  in  the  pulse,  allows  time  for  more 
blood  to  flow  out  of  the  arterial  system  through  the  capillaries,  and  when 
the  next  contraction  of  the  heart  occurs,  it  finds  the  arterial  pres- 
sure considerably  decreased,  and  it  is  now  able  to  open  the  valves  and 
cause  another  pulse-wave  to  pass  through  the  arteries." 


2  70 


Diseases  of  tJie  Heart. 


In  some  cases  the  irregularities  occur  at  fixed  intervals, 
i.e.  every  two,  three,  or  four  beats.  One  of  the  most  inte- 
resting- of  these  is  the  pulsus  bigcuiinus  of  Traube,  in  which 
the  pulse  waves  run  in  pairs.  (See  figs.  109  and  1 10.)  In  other 
cases  three  pulsations  occur  together  in  a  group,  constituting 
the  so  called  pulsus  trigcuii)ius.     (See  fig.  in.) 


Fig.    109. — Pulsus  bige minus 


Fig.    1 10. — Pulsus  bis^oninus. 


Fig.    1 1 1 . — Pulsus  tris^eniimus. 


Irregularity  in  volume.  —  Irregularities  in  volume  (see 
fig.  112)  depend  upon  the  fact  that  unequal  quantities  of 
blood  are  discharged  into  the  arterial  system  at  different 
contractions  of  the  left  ventricle.  The  condition  is  usually 
associated  with  irregularity  in  time,  for  when  the  time 
between   the  ventricular  contractions  varies,   the  amount  of 


Irregularity  of  tJie  Pulse.  271 

blood  which  the  left  ventricle  has  to  discharge  will  be  apt  to 
vary  too. 


KiG.     112. 

Differences  in  the  sphyginograpliic  cJiaracters  of  ijidividiial 
pulse  waves  depend  upon  differences  in  arterial  tension,  which 
in  their  turn  may  be  due  either  to — 

I.  Different  quantities  of  blood  being  propelled  during 
successive  contractions  of  the  left  ventricle  into  the  arterial 
system,  the  causes  of  which  condition  I  have  already 
considered. 


Pressure  3f  oz. 

Fig.    113. —  Uneven    Respiratory   Line. — J.    R.,   ret.    31,  admitted  to  Newcastle 
Infirmary  26th  December  1878,  suffering  from  acute  bronchitis. 

2.  The  effects  of  respiration.  During  tranquil  respiration 
the  respiratory  or  base  line  is,  as  I  have  previously  stated,  a 
straight  line.  During  deep  inspiration  and  expiration,  even 
in  health,  and  in  many  pathological  conditions  in  which  the 
respiratory  movements  are  profoundly  affected,  the  '  base 
line'  becomes  very  uneven  (see  figs.  113  and  1 14),  and  the 
sphygmographic    character    of    successive    pulse    waves    is 


272 


Diseases  of  the  Heart. 


different  ;  expiration  increases  the  pulse  tension  and  lessens 
the   frequency   of  the   pulse  ;  inspiration   lowers   the  tension 


and  increases  the  Ac 


qucnc}' 


Fig.    114.  —  Uneven  Respirato)y  line  (/rem  a  Case  of  Spasmodic  Asthma). 
The  tracing  was  taken  during  the  paroxysm. 

In  extreme  cases  the  pulse-wave  may  be  entirely  absent 
during  inspiration.  This  is  the  pulsus  paradoxicus  of  Kuss- 
maul.  The  most  striking  examples  of  this  condition  are  seen 
where  fibrous  adhesions  pass  between  the  thoracic  parietes 
and  the  roots  of  the  aorta  and  great  vessels.  During  a  full 
inspiration  these  fibrous  bands  are  stretched,  the  vessels  are 
constricted,  and  the  pulse-wave  is  unable  to  reach  the  wrist. 

The  pulsus  paradoxicus  has  also  been  noted  in  cases  of 
pericarditis  without  constricting  adhesions  ;  also  in  cases  of 
stenosis  of  the  air-passages. 


I 


Fig.  115.  —  Geyieral  Atheroma. — J.  I),,  at  60,  admitted  to  Newcastle  Infirmary 
2 1  St  October  1878.  The  radials  were  very  tortuous  and  rigid  ;  there 
was  no  valvular  lesion       The  tidal  wave  only  occurs  every  alternate  beat. 

3.  Differences  in  the  resistance  which  the  blood  stream 
meets  with  in  the  peripheral  vessels.  This  cause  is  proba- 
bly rare,  but  it  is  difficult  to  account  for  such  a  pulse  tracing 

'  At  the  beginning  of  inspiration  the  arterial  pressure  falls  ;  it  soon,  howe\er, 
begins  to  rise,  but  does  not  reach  the  maximum  until  some  time  after  expiration 
has  begun.  The  fall  continues  during  the  remainder  of  expiration,  and  passes  on 
itito  the  succeeding  inspiration  (Foster,  page  344).  In  speaking  of  the  cause  of  the 
respiratory  undulations,  Foster  says,  *  We  may  conclude  then,  that  the  respiratory 
undulations  of  blood-pressure  are  of  complex  origin,  being  partly  the  mechanical 
results  of  the  thoracic  movements,  possibly  also  produced  by  the  alternate  expan- 
sion and  collapse  of  the  pulmonary  alveoli,  but  probably,  in  addition,  brought 
about  by  a  rhythmical  variation  of  the  vascular  peripheral  resistance,  the  result  of 
a  rhythmical  activity  of  the  vasomotor  centre. ' —Third  edition,  p.  348. 


Irregiilaritv  oj  the  Pulse.  2y2> 

as  that  shown  in  fig.  115),  unless  we  suppose  either  a  rh}'th- 
mical  difference  in  the  strength  of  the  successive  cardiac  con- 
tractions, or  a  rhythmical  difference  in  the  peripheral  resist- 
ance ;  in  both  cases  the  primary  cause  is  evidently  nervous, 
and  I  see  no  reason  why  a  rhythmical  alteration  in  the  peri- 
pheral resistance  due  to  vaso-motor  causes  might  not  occur. 

TJic  clinical  significance  of  inequalities  of  rhythm  depends 
entirely  upon  the  cause  of  the  condition.  Occurring /^r  j-^, 
without  any  associated  signs  and  symptoms  of  disease,  the 
condition  is  of  no  practical  importance.  When  there  are 
other  signs  and  symptoms  the  prognosis  depends  entirely 
upon  their  cause. 

The  chief  pathological  conditions  associated  luith  irregu- 
larities in  time  and  volume  are — 

I.  Functional  derangements  of  the  heart,  such  as  are  pro- 
duced by  hysterical  conditions,  venereal  excess,  gout,  tobacco, 
tea,  etc. 

Physiologists  have  shown  that  when  the  excised  heart  is  fed  with 
rabbit's  serum  its  action  is  apt  to  become  intermittent.  This  in- 
termittence  is  possibly  due  to  the  chemical  action  of  the  serum. 
'Various  chemical  substances  in  the  blood  ("natural  or  morbid),'  says 
Michael  Foster,  'may  thus  affect  the  heart's  beat,  by  acting  on  its 
muscular  fibres,  its  reflex  or  automatic  ganglia,  or  its  intrinsic  inhibitory 
apparatus.'  ' 

2.  Mitral  lesions,  both  stenosis  and  regurgitation,  especially 
after  compensation  has  failed.   (See  figs.  116,  117,  118  and  1 19.) 


l^iessiire  3|  oz. 
I-IG.  116. — Irregularity  of  the  pulse. — W.  M.,  a-t.  50,  admitted  to  Newcastle  In- 
firmary 30th  November  1S78,  suflering  from  the  usual  symptoms  of  mitral 
disease.  The  heart's  action  was  extremely  irregular.  The  left  ventricle 
was  much  hypertrophied.  There  was  no  iheumatic  history.  The  symptoms 
were  of  two  months'  duration. 

'  A  Text-Book  of  Physiology,  third  edition,  p.   178. 
S 


2  74 


Diseases  of  the  Heai't. 


Fu;.  117. 
Figs,  i  16  and  117  were  two  consecutive  tracings  taken  on  loth  December,  after  the 
patient  had  improved  under  digitalis      The  intermittent  action  of  the  heart 
is  well  shown  in  fig.   117 


Fig, 


Pressure  4  oz 
118  — Mitral  Regurgitation. — S   B  ,  jet.  58,  admitted  to  Newcastle  Infirmary 
25th  February   1878,   suffering  from   cardiac  dropsy.     There  was   a   well- 
marked  mitral  systolic  murmur,  which  disappeared  under  treatment.     The 
heart  was  considerably  enlarged  (hypertrophied  and  dilated). 


I 


Press t4it  3  oz 

Fig.    119. — Irregular  and  Jnterinitteitt  Pulse — O.   M  ,  £Pt.    40,  admitted   to  the 

Newcastle  Infirmary  suffering  from  cardiac  dropsy.     The  heart  was  very 

much  enlarged  ;  apex  beat  4^^  inches  below  and  3  inches  outside  left  nipple ; 

systolic  mitral  murmur. 

There  has  been  a  good  deal  of  debate  with  regard  to  the  rhythm  of 

the  pulse  in  mitral  stenosis.     The  majorit)'  of  observers  are,  however. 

agreed — and   with    their   opinion    I    entirely   concur — that    the   pulse    is 

irregular.     Dr  Sansom — than  whom  no  better  authority  could  be  quoted — 

says,   '  We  may  conclude,  therefore,  that  a  pulse  tracing  which  shows 

irregularity  in  the  diastolic  periods,  sometimes  missed  pulsations,  and, 

as   described   by   Dr   B.    Foster,  the   occasional   appearance  of  a  small 

abortive  pulsation  in  the  line  of  descent,  is  very  strong  evidence  of  the 

existence  of  mitral  stenosis.' — {Diagtiosis  0/  Diseases  0/  the  Heart,  p.  269.) 

Dr  Mahomed,  who  was,  I  believe,  the  first  to  describe  this  peculiar  rhythm 

as  characteristic  of  mitral  stenosis,  has  since  somewhat  modified  his  views. 


The    Vol  It  me  of  the  Pulse.  275 

He  says,  'Although  it  is  very  commonly  present  in  this  disease,  perhaps 
more  commonly  than  in  any  other  valvular  lesion,  nevertheless  it  is  not  so 
much  a  sign  of  stenosis  of  the  valves  as  of  dilatation  of  the  ventricle.  It 
is  true,  that  in  the  typical  cases  of  mitral  stenosis  the  ventricle  is  not  dilated, 
but  I  am  unable  to  say  whether  this  irregularity  only  occurs  in  cases  in 
which  dilatation  exists.' — Gufs  Hospital  Reports,  1879,  p.  401. 

3.  Degenerations  of  the  cardiac  walls.  In  cases  of  fatty 
and  fibroid  degeneration,  and,  in  fact,  in  all  conditions  in 
which  there  is  much  degeneration  of  the  left  ventricle,  the 
heart's  action  may  be  very  irregular. 

4.  Some  affections  of  the  central  nervous  system,  such  as 
meningitis,  in  which  alterations  in  the  condition  of  the  intra- 
cranial circulation,  such  as  result  from  sudden  changes  in 
position,  etc.,  may  cause  alterations  in  the  rhythm  as  well  as 
in  the  rate  of  the  heart's  contractions. 


THE  VOLUME  OF  THE  PULSE. 

The  vohnne  of  the  pulse,  which  depends  upon  —  (i)  the 
size  of  the  artery  (radial,  carotid,  etc.)  which  is  being  ex- 
amined ;  (2)  the  amount  of  blood  which  is  propelled  into  the 
artery  at  each  ventricular  systole  ;  and  (3)  the  tonicity  of  the 
arterial  wall,  i.e.  the  condition  of  the  vaso-motor  apparatus, — 
may  be  appreciated  by  the  finger,  but  is  accurately  measured 
by  means  of  the  sphygmograph. 

In  hcaltJi  the  volume  of  the  pulse  varies  from  time  to  time, 
and  is  of  course  different  in  different  individuals.  There  are 
also  many  modifications  in  disease. 

A  laro;e  pulse,  i.e.  a  pulse  of  large  volume,  is  seen  in  the 
following  conditions  : — 

I.  In  many  cases  of  fever  during  the  earlier^  periods  of  the 
attack,  when  the  heart  is  acting  powerfully,  and  propelling  a 
large  quantity  of  blood  into  vessels,  the  tonicity  of  which  is 
already  somewhat  relaxed.'^ 

'  During  the  stage  of  rigor  the  pulse  is  small. 

^Towards  the  termination  of  cases  of  fever,  i.e.  after  the  contlition  lias  con- 
tinued for  some  time,  the  pulse  vessels  become  still  more  relaxed,  and  the  pulse 
becomes  small.      It  is  often  under  these  circumstances  dicrotic. 


276 


Diseases  of  the  Huari. 


2.  In  atheroma,  when  the  elasticity  of  the  arterial  walls  is 
impaired  and  the  vessels  are  dilated. 

3.  In  some  cases  of  hypertrophy,  and  in  some  cases  of 
simple  cardiac  excitement.     (See  figs.  120  and  121.) 

4.  In  aortic  regurgitation  the  systolic  portion  of  the 
tracing  is  of  large  volume,  but  the  diastolic  extremely 
small. 


Press ui-e  2^  cz 

Fig.  I20  — .Alteratw7ts  in  the  Piihe-traciu^s  as  the  result  of  Caruiac  Excitement  — 
A  M,  set  48,  admitted  to  the  Newcastle  Infirmary  suffering  from  obscure 
spinal  symptoms.  The  heart  became  excited,  and  the  tracing  shown  in 
fig.  120  was  taken  immediately  after  that  shown  in  fig  73,  the  instrument 
in  the  meantime  remaining  in  situ  The  spring  pressure  was  the  same  in 
each  case 


J'ressitre 


Fig.    121  — Hypertrophy  of  Left  Ventricle  —  A.  T  ,  an.  54,  admitted  to  Xewcasth 
Infirmary  suffering  from  cirrhotic  kidney. 


A  small  pulse  is  met  w  ith  : 

I.  In  those  conditions  in  which  the  amount  of  blood  dis- 
charged by  the  left  ventricle  is  below  the  normal  amount. 
Under  this  head  are  comprised  : — 


The    Tension  of  the  Pnlse. 


277 


{a)  Cases  (such  as  inanition)  in  which  the  total  amount  of 
blood  in  the  body  is  reduced  in  quantity.  (See 
fig.  122.) 

{b)  Cases  of  mitral  disease,  more  especially  regurgitation 
and  stenosis  after  the  failure  of  compensation.  (See 
fig.  123.)  In  the  former  (mitral  stenosis)  the  left 
ventricle  does  not  receive  the  usual  (normal)  amount 
of  blood  from  the  auricle  ;  in  the  latter  case,  some 
of  the  blood  which  ought  to  be  discharged  into 
the  aorta  flows  back  into  the  auricle  through  the 
incompetent  valve. 


Pressure  2  oz. 

Fig.  122. — Small  Weak  Pulse. — ^J.  M.,  set.  18,  a  soldier,  admitted  to  the  New- 
castle Infirmary  23d  January  1879,  suffering  from  abscess  of  the  liver  and 
pericarditis.     The  heart  was  displaced  upwards  and  to  the  left. 


Pressure  3  oz. 

Fig.  123. — Mitral  Regurgitation. — M.  A.  C,  ast.  16,  admitted  to  Newcastle  In- 
firmary 24th  January  1878,  suffering  from  cough  and  shortness  of  breath, 
dating  from  an  attack  of  rheumatic  fever  two  months  previously.  Heart's 
action  very  rapid  (120-130).  The  first  sound  appeared  to  be  reduplicated  ; 
a  systolic  murmur  at  the  apex,  audible  when  the  heart  became  slower. 

{c)  Cases  of  aortic  stenosis(see  fig.  124);  the  size  of  the  pulse 
being  in  proportion  to  the  narrowing  of  the  orifice. 


Pressure  \\  oz. 

Fig.  124. — Aortic  Stenosis. — J.  B.,  set.  51,  admitted  to  Newcastle  Infirmary  29th 
November  1878,  suffering  from  anaemia  and  dropsy.  There  was  a  well- 
marked  aortic  systolic  murmur  ;  the  left  ventricle  was  not  hyptrtrophied. 
The  pulse-tracing  seems  to  show  that  the  murmur  was  organic. 


278  Diseases  of  the  Heart. 

{d)   Conditions   of  cardiac   debility,  both   temporary   and 
permanent.  (See  fig.  122)  Conditions  of  collapse  are 
good  examples  of  the  former  ;  the  pulse  in  collapse 
being  small   and    thready,  while    fatty   and    fibroid 
degeneration  of  the  left    ventricle,  with    dilatation, 
are  types  of  the  latter. 
2     In   those  cases  in   which   the  vessels  are   unduly  con- 
tracted, as  in  peritonitis,  the  cirrhotic  form  of  kidney  disease, 
and  the  cold  stage  of  fevers,  i.e.  during  the  rigor. 

The  Compressibility  or  Strength  of  the  Pulse 
is  a  point  of  great  practical  importance,  for  in  many  cases  it 
indicates  the  condition  of  the  vaso-motor  nerve  apparatus, 
and  hence  of  the  general  tone  of  the  system. 

The  strength  of  the  pulse  is  measured  by  the  finger  or  by 
means  of  the  sphygmograph,  the  amount  of  pressure  required 
to  obliterate  the  pulse-wave  being  (provided  the  arterial 
walls  are  healthy)  the  true  indication  of  the  pulse-strength.^ 

Dr  Mahomed  gauges  high  tension  in  the  following  man- 
ner:—  'A  line  must  be  drawn  from  the  apex  of  the  up-stroke 
to  the  bottom  of  the  notch  preceding  the  dicrotic  wave  (fig. 
125,  A  C).    No  part  of  the  tracing  should  rise  above  this  line  ; 


(After  Afa/ioined.) 

Fig.  125. — Afa/iflii/€d\<:  method  of  gauging  high  tension.      The   tidal  wave   rises 

above  the  dotted  line  drawn  from  the  apex  A,  to  the  aortic  notch  C. 

if  it  does,  then  the  pulse  is  one  of  high  pressure.  The  height 
of  this  notch  is  another  good  gauge  of  pressure  ;  the  higher  it 
is  from  the  base  line  of  the  tracing  the  higher  is  the  pressure, 
the   nearer  it  approaches  the  line  the  lower  is  the  pressure. 

'  When  the  arterial  walls  are  inelastic  and  rigid,  as  in  cases  of  atheroma,  the 
amount  of  pressure  required  to  obliterate  the  pulse  is  not  a  true  criterion  of  its 
strength,  for  a  certain  (often  a  considerable)  amount  of  pressure  must  be  applied 
before  any  influence  is  exerted  upon  the  blood  wave  itself. 


The    Tension  of  the  Pulse.  279 

Lastly,  the  duration  of  systole  compared  to  that  of  diastole 
may  perhaps  be  reckoned  an  important  sign.'  Dr  Mahomed 
believes  '  that  there  is  a  normal  length  of  systole  for  a 
pulse  of  a  given  frequency,  and  that  the  length  of  the  systole 
is  increased  if  the  arterial  pressure  is  increased.'^ 

I  am  in  the  habit  of  considering  a  pulse  of  high  tension 
as  synonymous  with  a  strong  pulse,  and  vice  versa  a  pulse  of 
low  tension  v/ith  a  weak  pulse. - 

In  vigorous  health  the  strength  or  tension  of  the  pulse  is 
considerable,  but  there  are  great  differences,  even  in  persons 
who  present  all  the  external  appearances  of  good  health  ;  while 
alterations  in  the  tension  of  the  pulse  are  common  in  disease. 

A  pulse  of  higJi  tension  may  be  either  large  or  small,  the 
pulse  of  chronic  Rright's  disease  (especially  the  cirrhotic 
form),  in  which  the  heart  is  notably  hypertrophied,  is  illus- 
trative of  the  former  ;  the  pulse  of  peritonitis  is  an  excellent 
example  of  the  latter. 

A  ivcak  pulse,  or  pulse  of  lozv  tension,  is  also  very  common 
in  disease,  and  is  also  of  great  importance.  A  pulse  of 
low  tension  is  usually  associated  with  feeble  action  of 
the  heart  and  a  relaxed  condition  of  the  blood  vessels. 
It  may  be  either  small  or  large ;  the  former — a  small 
pulse  of  low  tension— is  seen  in  mitral  lesions  and  towards 
the  terminal  period  of  fever;  the  latter — a  large  pulse 
of  low  tension — is  also  seen  in  some  cases  of  fever  (as 
for  instance  in  certain  stages  of  rheumatic  fever),  and  in 
many  persons  who  enjoy  apparent  good  health,  but  in  whom 
the  vaso-motor  tone  is  below  par. 

As  a  general  rule,  a  slow  pulse  is  a  pulse  of  higher  tension 
than  a  quick  pulse,  and  vice  versa,  but  such  a  relationship  is 
by  no  means  constant  or  necessary. 

'   Gnys  Hospital  Reports,  1879,  p.  371. 

"  I,  therefore,  differ  from  Dr  Mahomed,  who  considers  that  hardness  or 
incompressibiliiy  is  the  least  constant  character  of  the  high  pressure  pulse.  '  It 
is  not  unfrequent,'  he  snys,  'to  find  tw^r/)/// vessels  associated  with  a  weak  or 
failing  heart,  the  pulse  is  then  often  small  and  feeble,  it  is  very  easily  com- 
pressed, and  is  described  as  a  small  weak  pulse,  which  is  thought  usually  to 
require  stimulants  ;  the  reverse,  however,  is  the  case  ;  bleeding  or  purging  will 
be  well  burne  by  such  patients,  and  the  result  will  be  most  satisfactory,' 


28o  Diseases  of  the  Heart, 

The  clinical  significance  of  the  tension  of  the  pulse. — The 
tension  of  the  pulse  is  of  great  importance,  both  for  diagnosis, 
prognosis,  and  treatment.  Dr  Mahomed,  for  example,  has 
shown  that  in  many  cases  of  chronic  Bright's  disease  there 
is  in  all  probability  a  stage  of  the  disease  in  which  the  urine 
is  healthy  (free  from  albumen,  casts,  etc.),  but  in  which 
there  is  persistent  high  arterial  tension,  and  further,  that 
by  reducing  this  condition  of  high  tension  the  subse- 
quent structural  affection  of  the  kidney  may  be  prevented. 
So,  too,  a  hard  pulse  associated  with  cardiac  pain  (angina 
pectoris)  indicates  a  serious  condition,  and  urgently  calls  for 
treatment. 

On  the  other  hand,  a  pulse  of  low  tension  is  no  less 
important  both  for  prognosis  and  treatment.  Persons  whose 
vaso-motor  tone  is  below  par,  i.e.  who  have  weak  pulses, 
bear  severe  (especially  acute)  disease  badly  ;  while  a  weak, 
and  especially  a  dicrotic  pulse  in  a  case  of  fev^er,  requires 
the  free  use  of  stimulants. 

The  Sphygmographic  Characters  of  the  in- 
dividual Pulse-waves. — Most  of  these  points,  which  are 
of  considerable  practical  importance,  such  as  dicrotism,  have 
been  already  fully  considered;  the  following  must  also  be 
observed:  — 

(i)  The  relative  duration  of  those  portions  of  the  tracing 
which  correspond  to  the  ventricular  systole  and  diastole.— -\n  the 
normal  condition  the  ventricular  systole  occupies,  as  we  have 
previously  seen,  about  ^^  of  the  entire  cardiac  revolution. 
This  relationship  is  altered  in  certain  cases  of  disease.  When 
the  heart  is  acting  very  rapidly,  the  diastole  is  relatively  more 
reduced  than  the  systole,  and  the  proportional  duration  of  the 
systolic  to  the  diastolic  portion  of  the  tracing  is  increased. 
Increased  temperature  of  the  blood,  has,  as  Dr  Paul  Chap- 
man ^  has  shown,  a  distinct  influence  in  shortening  the  dura- 
tion of  the  ventricular  systole;  and  the  same  authority  has 
observed,  on  coming  out  of  a   Turkish  bath,  'that  although 

^  B litis h  .Medical  Journ-il,  August  1 9,  1 882,  p.  300. 


Character's  of  Individual  Pulse  Waves.  281 

the  pulse-frequency  may  actually  increase,  the  systole  length- 
ens as  the  patient  cools.'  So,  too,  in  aortic  regurgitation,  the 
systolic  portion  of  the  tracing  is  usually  longer  than  the 
diastolic. 

(2)  The  relative  conditioti  of  the  vessel  (as  regards  its  ful- 
ness) during  systole  and  diastole. — In  some  cases  the  systolic 
portion  of  the  tracing  is  relatively  very  much  larger  than  the 
diastolic.  A  good  example  of  this  condition  is  seen  in  aortic 
regurgitation  (see  fig.  126),  in  which  the  artery  is  fully  dis- 
tended during  systole,  but  comparatively  very  empty  during 
diastole. 


Pressure  2j  oz. 

Fig.  126. — Aortic  Regurgitaticn. — Case:  G.  A. ,  ast.  56,  admitted  to  Newcastle 
Infirmary  21st  February  1878,  suffering  from  shortness  of  breath  and  swell- 
ing of  feet.  Had  been  ill  for  three  months.  The  face  was  pale  and  anxious, 
lips  slightly  dusky.  Double  aortic  murmur ;  heart  considerably  hyper- 
trophied  ;  apex  between  6th  and  7th  ribs,  3  inches  below  and  2  inches  out- 
side left  nipple.  Considerable  hypertrophy  and  engorgement  of  right  heart. 
Died  5th  March  1878.  Aorta  very  atheromatous  ;  aortic  valves  very  in- 
competent ;  segments  shrunken,  turned  in  towards  the  ventricle  ;  coronary 
arteries  much  obstructed  ;  cardiac  walls  fatty  ;  left  ventricle  dilated  ;  peri- 
cardium adherent.  The  arteries  were  practically  empty  during  the  ventri- 
cular diastole.  a-(^=upstroke  ;  iJ=apex  ;  f=tidal  wave  ;  d  indicates  the 
position  of  the  aortic  wave,  which  is  absent  in  this  tracing. 

An  empty  condition  of  the  arterial  system  during  the 
ventricular  diastole  is  often  associated  with  a  failing  heart,  and 
is  a  serious  indication  (see  figs.  127  and  128). 

When  the  pulse  \s  fully  dicrotie,  the  artery  at  the  point  of 
observation  is  apparently^  as  empty  at  the  end  as  it  is  at  the 
beginning  of  the  ventricular  systole,  and  is  apparently  more 
empty  at  the  end  of  the  ventricular  systole  than  it  is  during 
the  ventricular  diastole.     Again,  in  hyperdicrotism  the  artery 

'  See  foot  note  on  page  255. 


282 


Diseases  of  (he  Heart. 


at  the  point  of  observation  is  apparently  still  more  empty  at 
the  end  of  the  ventricular  systole. 


Fig.  127. — P}-essttre  2  oz. 


Fu;.  118. — Pressure  2^  oz 


Fig.  127. —  Weak  Pulse. — R.  R.,  x\..  17,  admitte  I  to  Newcastle  Infirmary  2 1st 
February  1878,  sutiering  from  iilii^pathic  anaemia.  Died  12th  April.  There 
was  a  systolic  (antemic)  mitral  murmur.  The  pulse-tracing  resembles  that 
of  mitral  regurgitation  (see  tig.  104).     Tracing  made  23d  February. 

Fig.  12S. — Pros^ressive  Pernicious  Anctvtia. — .Same  patient  (see  fig.  127).  Tracing 
taken  19th  March.     The  artery  is  almcjst  empty  during  diastole. 

In  other  cases  on  the  contrary  (in  chronic  Bright's  disease, 
for  example),  the  diastolic  portion  of  the  tracing  is  unduly 
sustained.  A  persistent  pulse  is  usually  a  pulse  of  high 
tension,  and  vice  versa  a  pulse  uhich  rapidly  falls  away  under 
the  finger  is  a  pulse  of  low  tension. 

THE   CONDITION    OF   TDK   ARTERIAL   COATS. 

The  condition  of  the  arterial  coats  with  regard  to  the 
presence  or  absence  of  atheroma,  is  a  point  of  great  practical 
importance,  for  atheroma  of  the  superficial  arteries — the 
radial,  temporal,  etc., — is  almost  invariably  associated  with 
similar  disease  of  the  aorta,  and  very  often  with  disease  of 
the  cerebral  vessels.  The  presence  or  absence  of  atheroma 
may  be  of  diagnostic  importance,  as  for  example,  in  a  case 
in  which  the  diagnc^is  lay  between  an  aneurism  and  a  solid 
intrathoracic  tumour. 

Atheroma  in  the  superficial  vessels  is  indicated  by  :  — 
(i)  Rigidity  of  the  arterial  coats;  the  vessel  generally 
'  stands  out  like  a  cord,'  is  markedly  visible  and  tortuous, 
while  its  coats  feel  thick  under  the  finger.  To  determine 
whether  the  arterial  coats  are  actually  thickened  or  not,  the 
artery  should  be  firmly  compressed  and  emptied  by  one 
finger,  while  the  other  finger  searches  for  the  vessel  below 
the    compressed  point.      When  the  vessel  can  be  distinctly 


1 


Comparison  of  the  Two  Radials.  28 


J 


felt,  even  though  empty  of  its  contents,  its  walls  are  obviously 
thickened  and  diseased.  This  is  an  important  point,  for  all 
arteries  which  are  firm  and  hard,  and  which  stand  out  like 
cords,  are  not  thickened. 

(2)  The  presence  of  a  well  marked  tidal  wave,  the  tension 
of  the  pulse  being  high  {i.e.  the  pulse  with  difficulty  obli- 
terated) but  a  low  pressure  being  usually  required  for  the 
production  of  the  best  tracing  {i.e.  the  first  ventricular 
wave  being  very  easily  extinguished). 

The  Comparison  of  the  two  Radial  Pulses  is 
useful  in  the  diagnosis  of  some  cases  of  aneurism  and  intra- 
thoracic tumour.  The  two  pulses  must  be  compared  as 
regards  ;  {a)  their  synchronism  as  to  time  ;  {b)  the  character 
of  their  respective  pulse  waves. 

Differences  in  time  between  the  two  pulses  are  most  easily 
appreciated  by  the  fingers.  In  health  the  two  radial  pulses 
are  of  course  synchronous,  but  in  some  conditions  of  disease, 
as  for  example,  where  the  sac  of  an  aneurism  is  situated  in 
the  course  of  the  circulation,  the  pulse  wave  is  retarded,  and 
is  consequently  delayed  at  one  wrist. 

Differences  in  the  cliaracter  of  the  pnlsc  zvaves  in  the  tzuo 
wrists  may  also  be  detected  by  the  finger,  but  are  much 
more  accurately  observed  by  means  of  the  sphygmograph. 
The  precautions  which  should  be  taken  in  comparing  the 
two  pulses  have  been  already  described.     (See  page  244.) 

Differences  in  the  tivo  pnlses  may  be  due  to  : — 

1.  Irregular  distribution,  such  as  high  division  of  the 
radial  artery.  In  such  cases  there  is  a  notable  difference  in 
the  size  of  the  vessel  in  the  two  wrists,  or  indeed  it  may 
apparently  be  altogether  absent  on  one  side.  The  condition 
is  easily  recognised  by  observing  the  condition  of  the  brachial 
arteries  on  the  two  sides,  and  by  feeling  for  the  position  of 
the  abnormal  vessel. 

2.  The  presence  of  an  aneurismal  sac  in  the  course  of  the 
circulation  on  one  side.  The  alterations  produced  by  the 
passage  of  the  blood  wave  through  a  globular  elastic  aneu- 
rismal   sac,    consist    in    retardation    of   the    pulse-wave    and 


284 


Diseases  of  the  Heart. 


flattening  of  its  curves.  In  well  marked  cases  the  up-stroke 
is  sloping,  the  apex  rounded,  and  the  secondary  curves 
entirely  obliterated.  (See  figs.  129  and  130,  which  represent 
the  pulse  tracings  on  the  two  sides,  from  a  case  in  which  a 
large  aneurism  involved  the  axillary  artery  on  the  left  side  of 
the  bod}'.) 


Pressure  3  oz. 
Fig.    129. — Atieiirism  of  Left  Axillary  Artery  (left  radial  tracin;;). — L.  G.,  set. 
63,   admitted  to  the  Newcastle   Infirmary  7th   March    1878,   with  a  large 
aneurism  of  the  left  axilhry  artery.     The  apex  is  rounded;  all  the  curves 
are  obliterated. 


Pressure  3  oz. 
Fig.  130. — Aneurism  of  Left  Axillary  Artery  (right  radial ). — Right  radial  tracing 
for  the  same  patient.     The  pulse  is  intermittent,  but  all  the  curves  are  well 

marked. 


Fig.  131. — (Right  radial. )  Pressure  \oz.     FiG.  132. — (Left  radial. )  Pressu7-e\oz. 

Figs.  131  and  132.  —  Aneicrism  of  Ascenditig portion  of  Aortic  A7xh. — J.  D.,  aet. 
50,  admitted  to  Newcastle  Infirmary  sufTering  from  a  large  aneurism  of  the 
ascending  thoracic  aorta  and  atheroma.  There  is  no  important  difference 
between  the  two  pulses. 

Differences  in  the  pulse  tracings  from  the  two  wrists  are 
not  of  course  observed  in  all  aneurisms.  When  the  aneurism 
involves  the  aortic  arch  below  the  origin  of  the  innominate 
the  pulse-wave  in  the  two  wrists  is  the  same,  though  the 
sphygmographic  tracing  on  each  side  may  be  modified  ^  (each 


'  The  alteration  in  these  cases  is  seldom  so  great  as  in  aneurisms  more  peri- 
pherally seated  (aneurisms  of  the  innominate  or  subclavian  foi  example). 


CoDiparison  of  the    Tzvo  Ra dials.  285 

pulse-wave  being  affected,  quoad  its  curves,  in  a  like  degree). 
Figs.  131  and  [32  illustrate  this  point. 

Again,  it  may  so  happen  that  an  aneurism  is  situated  on 
the  vessel  of  each  side,  or  that  an  aneurism  is  so  filled  up 
with  clot  that  the  pulse-wave  is  very  little  if  at  all  affected  in 
its  passage  through  it.  Such  was  the  fact  in  a  remarkable 
case  of  multiple-aneurism  which  I  have  recorded  in  the 
Edtiibi/n^h  Medical  Jonmal  for  June  1878,  p.  1076.  The 
pulse-tracings  from  the  two  radials  were  in  that  case  almost 
identically  the  same.     (See  figs.  133  and  134.) 


Fig.  133. — (Right  radial. )  Pressure  l  oz.     Fig.  134. — (Left  radial).   Pressure  t^  oz. 

Figs.  133  and  l^A.  —  Case  of  Multiple- Aneurism. ~^\.  F.,  aet.  64,  admitted  to  the 
Newcastle  Infirmary  i8th  February  1878,  suffering  from  symptoms  of  intra- 
thoracic pressure.  Died  loth  March.  Post-?7iortem  showed  dilatation  and 
small  aneurism  of  aortic  arch.  Fusiform  aneurisms  of  the  innominate,  left 
common  carotid  and  left  subclavian  arteries,  just  above  their  origins.  The 
aneurisms  were  filled  with  firm  clots,  through  which  a  straight  narrow 
channel  for  the  blood  remained. 

When  the  aneurismal  sac  involves  the  transverse  portion 
of  the  aortic  arch  be':ween  the  innominate  and  the  left  sub- 
clavian (the  circulation  through  the  innominate  being  inter- 
fered with),  the  right  radial  pulse  is  normal,  but  the  left  may 
be  modified. 

When  the  aneurism  involves  the  innominate,  the  right 
subclavian,  or  right  axillary  artery,  the  right  radial  pulse 
presents  the  aneurismal  characters,  while  the  left  is  normal. 
Vice  versa  when  the  left  subclavian,  or  left  axillary  artery 
is  affected,  the  left  radial  pulse  will  be  modified,  but  the 
right  normal. 

The  alteration  in  the  two  radial  pulses  may  be  of  con- 
siderable diagnostic  importance  Figs.  135  and  1  36  represent, 
for  instance,  the  right  and  left  pulse-tracings  of  a  patient  who 
was   admitted    to    the    Newcastle-on-Tyne    Infirmary,    under 


286  Diseases  of  the  Heart. 

my  care,  suffering  from  dyspepsia.  There  was  no  complaint 
of  any  thoracic  trouble.  On  taking  a  tracing  of  the  left 
radial  (I  was  at  that  time  working  at  the  sphygmograph,  and 
taking  tracings  of  every  case  admitted  to  hospital)  I  was,  of 
course,  at  once  struck  with  its  aneurismal  character,  and  on 
careful  physical  examination  found  decided  dulness,  faint 
pulsation,  and  marked  accentuation  of  the  cardiac  sounds 
over  the  chest  at  a  point  corresponding  to  the  origin  of  the 
left  subclavian  artery. 


F'IG.  135. — (Leflradial).    Pressure  t,oz.      Fir,.  136. — (Right radial).   Pressure 2,^ oz. 

Figs.  135  and  136. — Aneurism  of  Left  Suhclavlan. — J.  M.,  aet.  50.  admitted  to 
Newcastle  Infirmary  5th  September  1878  ;  all  the  waves  in  the  left  tracing 
are  obliterated. 


Fig.  137. — (Right  radial.)  Pressure  2\oz.      Fig.  138.— (Left  radial.)  Pressure2\oz. 
Figs.    137  and   138. — Difference  in  the  radial  pulses,  the  result  of  pressure  by  an 

intra-thoracic  tumour  on  the  innominate  artery.     J.  F.,  Kt.  50,  admitted  to 

the  Newcastle  Infirmary  24th  January  1878. 

3.  The  pressure  of  a  tumour  (solid  or  aneurismal)  on  the 
vessels  of  one  side  (on  the  innominate,  or  left  subclavian  for 
example).     (See  figs.  137  and  138.) 

4.  Differences  in  the  calibre  of  the  ves.sels  on  the  two  sides 
(innominate  and  left  subclavian)  such  as  are  produced  by 
obliquity  oi  origin  due  to  disease  (aneurismal  dilatation  of 
the  aortic  arch,  etc.),  or  to  the  presence  of  an  atheromatous 
patch  at  the  mouth  of  the  vessel  or  in  its  course. 

5.  Local  disease  in  one  radial  artery. 

Asynclironism  of  tJic  radial  pulse  zvith  the  cardiac  con- 
tractions has  been  already  alluded  to.      (See  page  268.) 


The  Condition  of  the  J 'e nous  Svstenr.  287 


THE    EXAMINATION    OF   THE    VENOUS    SYSTEM. 

T  have  repeatedly  directed  attention  to  the  fact  that  many 
of  the  most  prominent  symptoms  in  cardiac  cases  are  due  to 
obstructed  venous  return  ;  in  mitral  cases,  for  example,  as  soon 
as  compensation  fails  the  whole  systemic  venous  circulation 
becomes  engorged,  with  the  results  which  will  be  afterwards 
described  in  detail.  In  cases  of  this  description,  the  engorge- 
ment is,  for  a  time  at  least,  passive  ;  but  should  the  tricuspid 
valve  become  incompetent,  either  as  a  secondary  consequence 
of  mitral  disease  or  as  the  result  of  primary  changes  in  the 
lungs  or  right  cavities  of  the  heart,  a  backward  or  regurgitant 
current  is  propelled  into  the  venae  cavae,  and  an  active  ob- 
struction to  the  venous  return  is  added.  Again,  in  some  cases 
of  thoracic  aneurism,  and  in  some  cases  of  solid  intra-thoracic 
tumour — conditions  which  are  sometimes  with  difficulty  dis- 
tinguished— the  return  current  through  the  superior  vena  cava 
is  interfered  with,  and  a  venous  congestion,  limited  to  the 
territory  of  that  vein,  is  produced.  It  is  obviously,  therefore, 
of  the  greatest  importance  to  ascertain,  in  all  cases  of  cardiac 
disease,  the  exact  condition  of  the  venous  circulation,  and 
this  we  endeavour  to  do: — 

(i)  By  observing  the  colour  of  the  skin  of  the  peripheral 
parts,  more  especially  of  the  ears,  lips,  nose,  fingers,  toes,  etc. 
— a  point  which  has  been  considered  in  treating  of  the 
physiognomy  of  the  case  (see  page  87). 

(2)  By  noting  the  presence  or  absence  of  dropsy  in  the 
subcutaneous  cellular  tissue  and  serous  cavities — a  point 
which  has  also  been  considered  (see  page  89). 

(3)  By  noting  the  presence  or  absence  of  symptoms 
pointing  to  venous  engorgement  of  the  internal  organs,  such 
as  the  lungs,  liver,  stomach,  kidneys,  brain,  etc. 

(4)  By  examining  the  physical  condition  of  the  large 
venous  trunks,  in  particular,  the  condition  of  the  jugular 
veins. 

Inspection,  palpation,  and  auscultation  are  the  chief 
means  which  are  employed  in  order  to  ascertain  the  condition 


288  Diseases  of  I  lie  Heart. 

of  the  superficial  veins.  When  a  venous  pulse  is  present 
valuable  information  is  in  some  cases  afforded  by  the  tracings 
obtained  of  it. 

Inspection  of  the  veins  of  the  neck. 

In  conditions  of  health,  more  especially  in  well  nourished 
individuals  and  during  tranquil  respiration,  the  external 
jugular  veins  are  scarcel}',  if  at  all,  visible.  During  forced 
expiration,  more  especially  in  thin  persons,  they  become 
distended  and  stand  prominently  out.  All  of  us  have  pro- 
bably noticed  the  great  distention  of  the  veins  of  the  neck 
in  some  of  our  public  singers  after  sustained  and  powerful 
efforts. 

Distention  of  the  ju^nlar  veins  is  of  common  occurrence  in 
disease,  and  is  produced  by  all  conditions  which  interfere  with 
the  return  of  blood  to  the  heart.  In  practice  we  find  that 
distention  of  the  jugular  veins  chiefly  depends  upon  the 
following  conditions  : — 

1.  Mitral  lesions. 

2.  Diseases  of  the  lungs  (such  as  cirrhosis,  emphysema,  etc.) 
which  interfere  with  the  passage  of  the  blood  from  the 
right  to  the  left  sides  of  the  heart. 

3.  Disease  of  the  right  side  of  the  heart. 

4.  The  pressure  of  aneurisms  and  solid  intra-thoracic 
growths  upon  the  superior  vena  cava. 

5.  Pericarditis  and  inflammation  of  the  cellular  tissue  of 
the  mediastinum. — In  some  cases  of  adherent  pericardium  and 
of  indicative  mediastino-pcricarditis,  the  current  of  blood  to  the 
heart  is  interfered  with  and  the  jugular  veins  are  distended. 

6.  Plugging  of  the  superior  vena  cava — an  extremely  rare 
condition,  which  is  generally  due  to  disease  of  the  venous 
coats,  produced  by  external  pressure,  e.g.  the  pressure  of  an 
aneurism  or  intra-thoracic  growth. 

In  distention  of  the  jugulars  due  to  the  central  causes,  i.e. 
to  disease  of  the  heart  or  lungs,  the  distention  is  not  constant 
but  varies  with  the  condition  of  the  respiration,  being  most 
marked  during  expiration,  least    marked    and    usually   com- 


Distention  of  the  Jiigula}'  Veins,  289 

pletely  absent  during  inspiration.  (The  distention  of  the  veins 
of  the  neck,  which  is  due  to  adherent  pericardium,  occurs 
during-  the  depression  of  the  chest  wall  which  corresponds  to 
the  systole  of  the  ventricles ;  the  distention  of  the  veins 
rapidly  collapses  and  disappears  during  the  diastole  of  the 
ventricles.  The  distention  is  due  to  the  fact,  that  during  the 
systolic  depression  of  the  chest  wall,  the  cavity  of  the  chest 
is  diminished  in  size,  and  a  mechanical  hindrance  offered 
to  the  return  current  of  blood  through  the  superior  vena 
cava.  During  the  diastolic  rebound,  on  the  other  hand, 
the  cavity  of  the  chest  is  suddenly  distended,  a  suction 
force  is  exerted,  and  the  previously  engorged  veins  are,  in 
consequence,  suddenly  emptied.  In  indurative  mediastino- 
pericarditis,  the  distention  of  the  veins  of  the  neck  is  due  to 
the  pressure  of  bands  of  inflammatory  adhesions  upon  the 
vena  cava  superior  ;  and  since  the  obstruction  only  occurs 
during  inspiration,  the  jugular  veins  become  distended,  in- 
stead of  collapsing,  during  inspiration,  as  they  do  in  health ; 
the  distention  rapidly  subsides  during  expiration,  that  is, 
when  the  constrictive  bands  are  relaxed,  and  the  obstruction 
to  the  blood  in  the  superior  cava  is  removed.)  Its  amount, 
too,  varies  with  the  position  of  the  patient.  When  sitting 
or  standing,  the  distention  is  less  than  when  lying  down, 
owing  to  the  fact  that  in  the  erect  position  of  the  head,  the 
return  of  the  venous  blood  to  the  heart  is  favoured  by 
the  force  of  gravity.  The  distention  is  usually  greater  on 
the  right,  than  on  the  left  side  of  the  neck,  and  is  generally 
much  more  apparent  in  the  external  than  in  the  internal 
jugulars.  Exceptions  to  both  of  these  statements  do,  how- 
ever, occasionally  occur.^ 

The  swollen  external  jugular  veins  have  often  a  knotted 
appearance,  the  irregular  enlargements  corresponding  to  the 
position  of  the  venous  valves. 

As  the  result  of  distention  of  the  external  jugulars,  the  face 
(more  especially  the  lips,  ears,  and  nose)  becomes  cyanotic, 
and    the   features    swollen,    but    the   swelling    is    never   very 

'  I  have  seen  a  case  of  tricuspid  regurgitation  in  which  the  distention  and 
pulsation  in  the  internal  jugulars  were  much  greater  than  in  the  external. 

T 


290  Diseases  of  t lie  Heart. 

great.^  In  consequence  of  the  venous  distention,  the  brain 
becomes  congested,  and  symptoms  of  carbonic  acid  poisoning, 
viz.,  drowsiness,  mental  obfuscation,  and  ultimately  coma,  are 
apt  to  supervene. 

When  the  distention  is  due  to  a  central  cause,  i.e.  to 
disease  of  the  heart  or  lungs,  the  venous  engorgement  is  not 
limited  to  the  territory  of  the  superior  cava,  but  its  effects 
are  also  seen  in  the  lower  extremities  and  great  organs 
of  the  abdomen,  i.e.  in  the  territory  of  the  inferior  cava. 
Indeed,  as  we  have  previously  seen,  swelling  of  the  feet 
is  the  first  symptom  in  many  of  these  cases,  and  is 
generally  observed  before  the  distention  of  the  jugulars  is 
noticeable. 

When  the  distention  depends  upon  a  local,  as  distinguished 
from  a  central  cause,  i.e.  upon  direct  obstruction  to  the  return 
current  through  the  superior  cava,  the  symptoms  and  signs  of 
venous  engorgement  are  of  course  limited  to  the  two  sides  of 
the  head  and  neck,  the  upper  extremities,  and  the  upper  parts 
of  the  thoracic  parieties.  When  the  obstruction  is  great,  and 
particularly  in  those  cases  in  which  it  is  complete,  the  parts  from 
which  the  superior  cava  draws  its  blood  may  become  remark- 
ably oedematous,  and  it  is  in  cases  of  this  description  that  the 
peculiar,  hard,  brawny  swelling,  to  which  the  terra  '  collar  of 
flesh,'  has  been  applied,  is  observed. 

As  I  have  previously  pointed  out,  the  swelling  df  the  face, 
which  is  due  to  obstructed  venous  return  through  the  superior 
cava  is  readily  distinguished  from  that  which  is  met  with  in 
renal  dropsy,  and  with  which  it  might  at  the  first  glance  be 
confounded,  by  the  facts  : — 

(i)  That  the  face  is  not  only  swollen  but  is  also  cyanotic. 

(2)  That  the  swelling  involves,  and  is  limited  to,  the  terri- 
tory of  the  superior  cava. 

(3)  That  there  is  no  kidney  disease. 

(4)  That  there  are  symptoms  and  signs  of  aneurism,  intra- 
thoracic growth,  or  other  local  pathological  condition  likely  to 
obstruct  the  vein  or  produce  disease  of  its  coats. 

'  The  swelling  is  never  so  great  as  in  cases  of  obstmctiun  of  the  superior  vena 
cava  from  direct  pressure. 


PiLlsation  in  t/ic  Jugulai^    Veins.  291 

Pulsation  in  the  jugular  vci)is. —  In  conditions  of  health 
there  is  no  perceptible  pulsation  in  the  jugular  veins,  but  in 
cases  of  disease,  rhythmical  undulations  and  pulsations,  more 
particularly  in  the  external  jugulars  are  sometimes  met  with. 
In  some  cases  these  pulsations  are  only  apparent ;  in  others 
they  are  real,  and  represent  a  true  venous  pulse. 

Apparent  pulsation. — When  the  jugulars  arc  distended,  as 
the  result  of  a  central  obstruction,  i.e.  of  disease  of  the  heart 
or  lungs,  a  rhythmical  undulation,  corresponding  in  time  to 
the  movements  of  inspiration  and  expiration,  is  generally 
observed.  The  vein  is  distended  during  expiration  and 
collapses  during  inspiration.  This  apparent  pulsation  is  at 
once  distinguished  from  a  true  venous  pulse  by  its  rhythm. 

In  indurative  mediastino-pericarditis,  as  has  been  described 
above,  an  'apparent'  pulsation  is  sometimes  seen  in  the  veins 
of  the  neck  ;  but  it  differs  from  the  ordinary  form  of  ap- 
parent pulsation,  inasmuch  as  the  vein  is  distended  during 
inspiration  and  empty  during  expiration. 

In  some  cases  of  adherent  pericardium,  the  veins  of  the 
neck  are  distended  during  the  systole  of  the  ventricles,  as  I 
have  described  above.  This  pulsation,  which  is  of  course  only 
apparent  and  due  to  simple  passive  distention,  must  be  dis- 
tinguished from  true  pulsation  of  tricuspid  regurgitation  in 
which  a  '  back-wash  '  is  propelled  into  the  veins  at  each  systole 
of  the  right  ventricle. 

In  other  cases,  undulations  which  correspond  in  time  to 
the  cardiac  contractions  are  observed.  In  some  of  these  the 
undulations  are  due  to  impulses  communicated  to  the  dis- 
tended veins  by  the  subjacent  arteries  ;  in  others,  they  are 
due  to  the  fact  that  the  contraction  of  the  right  auricle  com- 
municates an  impulse  or  shock  to  the  blood  in  the  superior  vena 
cava,  which  is  propagated  to  the  jugulars.  It  is  also  said  that 
the  contraction  of  the  right  ventricle,  even  when  the  tricuspid 
is  sound,  may  communicate  a  shock  through  the  tightly 
stretched  tricuspid  valve,  to  the  blood  in  the  right  auricle, 
which  may  be  propagated,  through  the  vena  cava  superior,  to 
the  jugulars.  It  is  improbable,  however,  that  any  marked 
undulation  in  the  jugulars  can  be  produced  in  this  way. 


292  Diseases  of  the  Heart. 

Apparent  pulsation  of  this  description,  i.e.  apparent  pulsa- 
tion of  the  jugular  veins  synchronous  with  the  contraction  of 
the  heart,  is  readily  distinguished  from  true  jugular  pulsation 
produced  by  a  back-wash,  i.e.  from  pulsation  indicative  of 
tricuspid  regurgitation,  by  compressing  the  vein  in  the  middle 
of  the  neck,  and  observing  the  condition  of  the  portion  of 
vein  which  is  placed  below  the  finger,  i.e.  between  the  heart 
and  the  compressed  point.  If  the  pulsation  is  real,  it  will 
still  be  observed  in  the  vein  below  the  finger,  for  with  each 
systole  of  the  right  ventricle  the  vein  is  again  filled  from 
below  by  the  back-wash.  If  the  vein  remains  collapsed  and 
empty,  the  pulsation  is  only  apparent. 

True  pulsation  of  systolic  rhytJnn  is  due  to  a  stream  of  blood 
being  propelled  into  the  vein  at  each  systole  of  the  right 
ventricle.  This  condition  is  of  extreme  importance,  and  in- 
dicates tricuspid  incompetence  ;  it  also  shows  that  the  valves 
at  the  point  of  junction  of  the  internal  jugular  and  subclavian 
veins  are  incompetent.  Jugular  pulsation  of  this  description 
ij.e.  true  jugular  pulsation  indicative  of  tricuspid  regurgitation), 
is  sometimes  associated  with  pulsation  of  the  inferior  vena 
cava,  the  effects  of  which  have  been  previously  described. 

The  exact  chararacter  of  the  jugular  pulse-wave  is,  as 
Friedreich  has  shown,  of  some  practical  importance.  In  an 
extremely  able  paper  on  '  The  Auricle  in  Health  and  Dis- 
ease,' Dr  Gibson  has  directed  attention  to  this  point ;  and  has 
figured  some  of  Friedreich's  tracings  (see  figs.  139,  140)     '  The 


Fig.  139.  Fig.  140. 

Fig.   139. — Jugular  pulse  tracing  showing  the  presence  of  the  auricular  wave  a. 

(After  Friedreich.) 
Fig.    140. — Jugular  pulse   tracing    after   paralysis   of  the    auricle  ;    the  auricular 

wave  a,  in  the  preceding  figure  is  no  longer  present.     (After  Friedreich.) 


Pulsation  of  the  Pei^ipheral   Veins.  293 

one  shows,'  he  says,  '  three  waves,  a,  b,  and  c  ;  the  other  only 
two,  b  and  c.  Bestowing  our  attention  mainly  upon  the  first 
wave,  a,  which  is  caused  by  the  systole  of  the  right  auricle, 
we  find  in  it  an  index  of  the  state  of  the  auricular  muscle. 
So  long  as  it  is  shown  in  tracings  from  the  jugular,  the 
auricle  is  comparatively  healthy  ;  when  it  disappears  it  is  a 
certain  proof  of  paralysis  of  the  auricle,  and  if  it  should 
reappear  it  gives  evidence  of  a  return  of  contractile  power. 
In  this  way  the  auricular  wave  in  the  jugular  veins  is 
of  very  considerable  practical  interest.  The  large  wave,  b,  is 
caused  by  the  systole  of  the  ventricle,  and  the  third  wave,  c,  is 
reflected  from  the  interior  of  the  heart,  in  the  same  way  as  the 
dicrotic  wave  in  the  radial  tracings  of  aortic  regurgitation  first 
shown  by  Naumann.'^ 

Tnie  pulsation  of  presystolic  rliytJun. — When  the  venous 
valves  are  incompetent  in  consequence  of  over-distention  of 
the  veins,  pulsation  of  presystolic  rhythm  is  sometimes  ob- 
served. It  is  produced  by  the  contraction  of  the  right  auricle 
and  may  occur  independently  of  any  systolic  'backwash' 
representing  tricuspid  regurgitation. 

Pulsation,  like  distention,  is  usually  more  marked  in  the 
right  than  in  the  left  side  of  the  neck,  and  is  generally  more 
perceptible  in  the  external  than  in  the  internal  jugulars. 

Pulsation  in  the  peripheral  veins,  such  as  the  veins  on  the 
back  of  the  hand,  is  occasionally  though  rarely  observed.  It 
is  seen,  for  instance,  in  some  cases  of  aortic  regurgitation,  and 
is  due  to  the  fact  that  the  pulse  wave  is  not  obliterated  in  the 
arteries  as  in  health,  but  passes  right  on  to  the  veins  through 
the  capillaries.  Prof  Michael  Foster  gives  the  following  lucid 
description  of  the  ways  in  which  it  may  be  produced  : — '  To 
recapitulate  :  there  are  three  chief  factors  in  the  mechanics  of 
the  circulation,  (i)  the  force  and  frequency  of  the  heart-beat, 
(2)  the  peripheral  resistance,  (3)  the  elasticity  of  the  arterial 
walls.  These  three  factors,  in  order  to  produce  a  normal 
circulation,  must  be  in  a  certain  relation  to  each  other.  A  dis- 
turbance of  these  relations  brings  about  abnormal  conditions. 

'  Edinburgh  Medical  Journal,  Aug.  1882,  p.  126. 


294  Diseases  of  the  Heart. 

Thus,  if  the  peripheral  resistance  be  reduced  beyond  cer- 
tain Hniits,  while  the  force  and  frequency  of  the  heart  re- 
main the  same,  so  much  blood  passes  through  the  capillaries ' 
at  each  stroke  of  the  heart  that  there  is  not  sufficient  left 
behind  to  distend  the  arteries,  and  bring  their  elasticity  into 
play.  In  this  case  the  intermittence  of  the  arterial  flow  is 
continued  on  into  the  veins.  An  instance  of  this  is  seen  in 
the  experiments  on  the  sub-maxillary  gland,  where  sometimes 
the  resistance  offered  by  the  minute  arteries  of  the  gland  is 
so  much  lowered,  that  the  pulse  is  carried  right  through  the 
capillaries,  and  the  blood  in  the  veins  of  the  gland  pulsates. 
A  like  result  occurs  when,  the  peripheral  resistance  remaining 
the  same,  the  frequency  of  the  heart's  beat  is  lowered.  Thus 
the  beats  may  be  so  infrequent  that  the  whole  quantity  sent 
on  by  a  stroke  has  time  to  escape  before  the  next  stroke 
comes.  Lastly,  if,  while  the  heart's  beat  and  the  peripheral 
resistance  remain  the  same,  the  arterial  walls  become  more 
rigid,  the  arteries  will  be  unable  to  expand  sufficiently  to  retain 
the  surplus  of  each  stroke  or  to  exert  sufficient  elastic  reaction 
to  carry  forward  the  stream  between  the  strokes  ;  and  in 
consequence  more  or  less  intermittence  will  become  manifest.'^ 

Palpation  uf  the  superficial  veins  is  not  a  method  of 
physical  examination  of  much  consequence,  except  in  those 
cases  in  which  the  vein  is  plugged  by  a  coagulum.  In  cases 
of  this  description,  the  vein  can  be  felt  as  a  firm  rigid  cord,  and 
there  is  usually  at  the  same  time  tenderness  on  pressure.  In 
cases  of  well  marked  venous  pulsation,  such  for  instance  as  is 
due  to  tricuspid  incompetence,  the  pulsations  can  be  felt  as 
well  as  seen.  In  some  cases  of  anaemia,  in  which  the  venous 
hum  which  I  shall  presentl}'  describe  is  well  marked,  a  thrill 
can  be  felt  when  the  finger  is  placed  over  the  veins  at  the 
root  of  the  neck. 

Auscultation  of  the  veins. — In  a  considerable  proportion  of 
cases,  even  in  apparent  health,  and  notably  in  conditions  of 
anaemia,  a  continuous  humming  murmur,  to  which  the  term 

'  A  Text  Book  oj  Fhysioloy.     P'ourlh  edition,  p.  131. 


AiLsciLltatioii  of  the    l^cins.  295 

bruit  de  diab/c,  or  huviniing-top  imirnmr,  has  been  given,  is 
heard  in  the  veins.  In  many  cases  it  closely  resembles  the 
roaring  sound  which  is  heard  when  a  shell  is  placed  close  to 
the  ear.  It  is  usually  best  heard  at  the  junction  of  the  internal 
jugular  and  sub-clavian  veins,  is  intensified  by  the  pressure 
of  the  stethoscope,  by  turning  the  head  forcibly  to  the  opposite 
side,^  and  by  a  deep  inspiration."^ 

The  murmur  is  generally  louder  on  the  right  side.  It  is 
usually  continuous,  but  in  some  cases  is  only  produced  on 
deep  inspiration,  and  in  such  cases  is,  therefore,  intermittent. 

In  conditions,  of  anaemia  venous  murmurs  may  be  often 
heard  in  other  situations,  as,  for  example,  over  the  torcular 
Herophili  and  eyeball. 

'  When  the  head  is  turned  to  the  opposite  side,  the  muscles  and  fascia  are  put 
upon  the  stretch,  the  vein  is  compressed,  and  its  channel  narrowed. 

^  A  deep  inspiration  quickeus  the  flow  of  blood  to  the  heart,  and  favours  the 
production  of  fluid  veins. 


296  Diseases  of  the  Heart. 


CHAPTER       IV. 

DISEASES  OF  THE  PERICARDIUM;  ACUTE  PERICARDITIS;  PERICARDIAL 
ADHESION;  INDURATIVE  MEDIASTINO  -  PERICARDITIS  ;  CHRONIC 
PERICARDITIS;   HYDROPERICARDIUM  ;   PNEUMOPERICARDIUM. 

Haying  made  ourselves  acquainted  with  the  introductory 
parts  of  our  subject  (the  anatomy,  physiology,  pathology, 
and  clinical  examination  of  the  heart),  we  are  now  in  a 
position  to  study  the  individual  diseases  in  detail.  It  will  be 
convenient  to  consider : — 

(i.)  The  diseases  of  the  pericardium. 

(2.)  The  diseases  of  the  endocardium. 

(3.)  The  diseases  of  the  myocardium. 

(4.)  The  neurotic  affections  of  the  heart,  which  include  the 
purely  functional  disorders  of  the  organ. 

(5.)  The  diseases  of  the  great  blood-vessels. 

The  congenital  malformations  of  the  heart,  which  are 
usually  treated  under  a  distinct  head,  will  be  described  under 
the  diseases  of  the  endocardium  and  myocardium. 

THE  DISEASES   OF   THE   PERICARDIUM. 

The  morbid  conditions  of  the  pericardium,  which  are  of 
practical  and  clinical  importance  are  : — 

1.  The  inflammatoiy  affections  and  their  results  (peri- 
carditis, adherent  pericardium,  indurative  mediastino-peri- 
carditis). 

2,  The  effusions  of  fluid  (of  a  non-inflammatory  character) 
into  the  sac  (hydropericardium,  haemopericardium). 


I 
I 


Pericarditis.  297 

3.  The  collections  of  air  or  gas  in  the  sac  (pneumo- 
pericardium). 

Coitgenital  deficiencies  and  malformations  (diverticula)  of  the  peri- 
cardium occasionally  occur,  but  are  seldom  suspected  or  recognised 
during  life.  In  a  few  cases  the  whole  pericardial  sac  has  been  absent, 
more  frequently,  limited  deficiencies  or  imperfections  in  it  have  been 
observed. 

New  groivtJis  (tubercles,  sarcomatous  and  cancerous  tumours)  occa- 
sionally affect  the  membrane  ;  and  parasites  and  free  bodies  (which 
usually  have  resulted  from  previous  inflammatory  deposits  or  new 
growths)  are  vzry  exceptionally  found  in  the  sac.  But  it  is  not  neces- 
sary to  describe  these  conditions  separately.  Unless  they  give  rise  to 
pericarditis  (which  they  frequently  do)  they  are  unattended  by  any  distinct 
symptoms  or  physical  signs,  and  cannot  be  recognised  during  life. 

PERICARDITIS. 
Definition. — Inflammation  of  the  pericardium. 

Like  all  other  forms  of  inflammation,  pericarditis  may  be 
either  acute,  sub-acute,  or  chronic.  As  a  matter  of  practical 
convenience  it  is  only  necessary  to  describe  separately  the 
acute  and  chronic  forms. 

ACUTE  PERICARDITIS. 
Definition. — Acute  inflammation  of  the  pericardium. 

Varieties. — Many  different  varieties  of  the  disease  may  be 
described.  We  may,  for  example,  make  an  aetiological  sub- 
division, and  divide  cases  of  pericarditis  into  two  great  groups, 
v\z.  primary  and  secondary,  and  then  again  subdivide  each  of 
these  groups  into  still  smaller  ones,  as,  for  instance,  into  cases 
of  tranviatic  pericarditis,  rhenmatic  pericarditis,  idiopathic 
pericarditis,  and  the  like.  Or,  we  may  make  a  pathological 
division,  in  accordance  with  the  extent  of  the  inflammation 
{diffuse  and  circumscribed'^  pericarditis),  or  in  accordance  with 
the  character  of  the  inflammatory  product  (Jibrinoiis,  purident, 

'  The  division  into  diffuse  and  circumscribed  is  theoretical  rather  than  practical, 
for  in  acute  pericarditis,  at  all  events,  the  inflammation  is  almost  invariably  diffuse. 


298  Diseases  of  the  Heart. 

hccmorrhagic,  etc).  Or  again,  \vc  may  take  a  clinical  (or 
rather  a  clinico-pathological)  basis,  and  divide  cases  of  peri- 
carditis into  dry  and  vwist,  in  accordance  with  the  amount  of 
effusion  and  the  condition  of  the  cardiac  dulness. 

Etiology. — Acute  pericarditis  may  occur  at  any  period  of 
life,  but  it  is  rarely  met  with  in  young  children  ;  it  is  most 
common  between  the  ages  of  fifteen  and  twenty-five.  It  is 
slightly  more  common  in  men  than  in  women,  and  is  most 
frequently  observed  in  persons  who  follow  outdoor  occupa- 
tions, more  especially  those  who  are  exposed  to  cold  and  wet, 
and  to  great  variations  in  temperature  ;  facts  which  are  pro- 
bably explained  by  the  circumstance  that  men,  and  especially 
men  who  are  exposed  to  cold  and  wet,  are  more  frequently 
affected  with  acute  rheumatism  than  other  members  of  the 
community.  In  women  it  is  much  more  common  amongst 
young  serv^ant  girls  and  washer-women  than  in  those  engaged 
in  any  other  occupation.  Over-action  of  the  heart  seems  to 
predispose  to  the  condition. 

Primary  pericarditis  is  extremely  rare.  It  may  be  due 
to:— 

(a)  Traumatic  injuries,  such  as  wounds  of  the  sac,  blows 
on  the  front  of  the  chest,  etc. 

(b)  Primary  new  growths  (sarcomata,  carcinomata,  etc.)  in 
the  pericardial  tissues.  These  primary  new  growths  are  ex- 
tremely rare. 

(c)  Exposure  to  cold  and  wet,  independently  of  acute 
rheumatism  or  of  any  other  diseased  condition.  This  is 
probably  the  rarest  of  all  the  causes  of  pericarditis.  The 
following  is  a  case  in  point ;  it  is  also  interesting  from  the  fact 
that  until  shortly  before  death  there  were  no  symptoms  in- 
dicative of  serious  disease. 

Case — Latent  idiopathic  pericarditis  j  death. 

A  girl,  jet.  17,  who  had  previously  enjoyed  good  health,  but  who  had 
never  menstruated,  complained  of  uneasiness  in  the  upper  part  of  the 
abdomen,  and  of  constipation.     The  tongue  was  slightly  furred,  the  pulse 


Aitiology  of  Acute  Pericarditis.  299 

a  little  quick,  but  there  was  nothing  to  direct  attention  to  any  serious 
disease  within  the  chest.  A  dose  of  castor  oil  was  prescribed,  and  nothing 
more  was  heard  of  the  case  for  a  few  days.  I  was  hurriedly  sent  for, 
and  found  the  patient  dead.  She  had  passed  a  somewhat  restless  night, 
but  had  got  up  to  breakfast  as  usual  ;  had  suddenly  complained  of  feeling 
faint,  and  had  fallen  back  dead.  All  the  organs  were  healthy,  with  the 
exception  of  the  heart.  The  pericardium  was  distended  with  turbid  fluid, 
and  both  surfaces  of  the  pericardium— both  visceral  and  parietal  layers — 
were  covered  with  a  layer  of  recent  lymph.  (See  fig.  141.)  The  case  was 
therefore  one  of  pericarditis  ;  and  syncope  was  the  immediate  cause  of 
death.  On  inquiry  I  ascertained  that  the  patient  had  waded  in  the  sea  a 
fortnight  previously,  and  that  for  some  days  afterwards  she  had  been 
a  little  hoarse.  There  was  no  histoiy  of  rheumatism.  So  trivial  were  the 
symptoms,  in  this  se\'ere  and  acute  case,  that  the  patient  was  able  to  go 
about  her  occupation — that  of  a  baker's  assistant — until  two  days  before 
her  death. 

Secondary  pericarditis  is  a  comparatively  common  condi- 
tion.    It  occurs  : — 

(a)  In  the  course  of  some  general  affections.  The  disease- 
par  excellence  with  which  it  is  associated,  and  of  which  it  is,  as 
it  were,  part  and  parcel,  is  acute  rheumatism.  Indeed,  a  large 
proportion  of  the  cases  of  acute  pericarditis,  met  with  in  prac- 
tice, are  rheumatic.  It  is  more  apt  to  occur  in  first  than  in 
subsequent  attacks  of  rheumatic  fever,  and  in  severe  rather 
than  in  mild  cases.  Pericarditis  also  occasionally  occurs  in 
the  course  of  scarlet  fever.  It  is  a  somewhat  common  com- 
plication in  Bright's  disease,  more  especially  the  cirrhotic 
form  ;  and  in  cases  of  that  description  is  not  unfrequently  the 
immediate  cause  of  death.  It  is  sometimes  met  with  in 
pyaemia,  purpura,  and  scurvy. 

(b)  As  the  result  of  the  direct  extension  to  the  pericardium 
of  an  inflammation  or  new  growth  which  has  originated  in 
some  of  the  adjacent  organs  or  parts.  This  is  one  of  the 
most  common,  probably  the  most  cominon  cause  of  peri- 
carditis which  proves  fatal  during  the  acute  stage.^  The 
primary  inflammation  or  new  growth  may  originate  in  the 
pleura,  lung,  bronchial  glands,  tissues  of  the  mediastinum, 
the  cellular  tissue  of  the  neck,  or  in  the  structures  below  the 

'  Rheumatic  pericarditis  is,  perhaps,  relatively  more  frequent,  but  is  very  seldom  fatal. 


300  Diseases  of  the  Heart. 

diaphragm,  i.e.  in  the  cavity  of  the  abdomen.  An  abscess 
of  the  Hver,  for  example,  may  by  direct  extension  through 
the  diaphragm  (and  without  bursting  into  the  sac)  give  rise 
to  an  inflammation  of  the  pericardium. 

(c)  As  the  result  of  secondary  deposits  of  a  tubercular, 
sarcomatous,  or  cancerous  nature  in  the  structure  of  the 
pericardium,  the  primary  new  growth  being  situated  at  a 
distance,  and  the  secondary  deposits  being  carried  to  the 
pericardium  by  the  veins  or  lymphatic  vessels. 

Pathology  and  Morbid  Anatomy. — The  naked  eye  and 
microscopical  appearances  which  are  seen  in  cases  of  acute 
pericarditis  vary  with  : — 

(i.)  The  extent  of  the  inflammation. 
(2.)  The  stage  of  the  inflammation. 
(3.)  The  amount  and  kind  of  exudation. 

The  extent  of  the  infiavimation. — In  the  great  majority  of 
cases  the  inflammation  is  general,  and  involves  the  whole 
extent  of  both  layers  of  the  pericardial  sac.  In  rare  cases  the 
inflammatory  process  is  limited  in  distribution.  In  recent 
cases  of  this  description,  the  chief  morbid  appearances  are 
usually  to  be  found  at  the  base  of  the  organ,  around  the  roots 
of  the  great  vessels  and  auricular  appendages.  In  other  cases, 
more  particularly  when  the  inflammation  is  of  some  duration 
or  has  become  chronic,^  inflammatory  adhesions,  of  limited 
extent,  are  found  at  or  near  the  apex,  on  the  posterior  surface, 
or  it  may  be  on  any  part  of  the  Organ. 

The  stage  of  tJie  infainniation,  and  the  amount  and  kind  of 
exudation. — In  pericarditis  the  primary  vascular  changes  (dila- 
tation and  stasis)  which  characterise  all  inflammations  are 
quickly  followed  by  the  pouring  out  of  inflammatory  exuda- 
tion matters  into  the  serous  cavity  or  sac. 

The  naked  eye  appearances  are  as  follows  : — 

In  the  earliest  stages,  which  it  must  be  observed  we  seldom 

'  To  avoid  repetition,  the  pathological  appearances  which  are  seen  in  sub-acute 
and  chronic  pericarditis  are  included  under  this  description. 


Fig.  141. 
Eearijrom  a  case  of  recent  Pericarditis.    (^Natural  size.) 

The  surface  of  the  organ  is  coated  with  lymph,  which  is  easily  detached.  The  letter,  a,  points 
to  a  portion  of  the  heart  covered  by  lymph;  b,  to  a  detached  shred  of  lymph;  c,  to  a  portion 
of  the  heart  from  which  the  lymph  has  been  removed. 


M'LA«»iCu«i<iNaliT> 


Fig.  142. — Front  view  of  the  heart  in  a  case  of  acute  pericarditis.     {Natural  size.') 

The  front  of  the  parietal  perirardiura,  which  was  verj-  much  thickened,  has  heen 
cut  away;  a  wedge-shaped  portion  has  heen  removed  froiri  the  apex  of  the  left 
ventricle  for  microscopical  examination. 

[^ote. To  be  seen  properly  this  di-awing  should  be  held  about  two  feet  from  tlie 

eve. 


^''*"  ^fhZ^vTvwlh  VZ  '?/'«^/?i'^'''"'-.«'-^''^^-  its  svrfa^e  is  covered v^M  l<n,g  fibres  of 
^^Note.~To  be  seen  properly  this  drawing  should  be  held  about  two  feet  from  the 


W^UMHiCuMMKje.bTwc?.  Ew 


Fm.  144. 
Heart  from  a  case  of  Pericarditis,  showing  vegetations  consisting  of  firm  lymph  on  its  exterior. 

{Natural  size.') 


Mn.u««Cu««i»c.lj'"o'E»' 


PatJiology  of  Acute  Pericarditis.  301 

have  an  opportunity  of  studying  on  \h&  post-mortem  table,  the 
membrane  is  seen  to  have  lost  its  normal  smooth,  glistening, 
appearance  ;  its  vascularity  is,  in  places  at  least,  increased  ; 
and  small  punctiform  ecchymoses  are  sometimes  to  be  seen. 
In  the  great  majority  of  cases  small  deposits  of  fibrine  can 
generally  be  perceived  by  the  naked  eye  ;  and  the  normally 
smooth  membrane  has  a  more  or  less  rough  feel  when  the 
finger  is  passed  over  it. 

In  a  few  hours,  the  exudation  becomes  more  copious.  The 
appearances,  which  are  seen  when  the  fiilt  development  of  the 
exudation  is  reached,  vary  greatly  in  different  cases. 

In  some  cases  the  amount  of  fluid  poured  out  into  the 
pericardial  sac  is  scanty,  in  others  copious.  In  most  cases  the 
exudation  is  sero-fibrinous,  and  instead  of  the  clear  serum 
which  is  normally  found  in  the  sac  of  the  pericardium  after 
death,  the  fluid  is  more  or  less  turbid,  and  contains  flakes  of 
coagulated  lymph.  In  others  it  is  blood  tinged,  much  more 
rarely  it  is  bloody  or  purulent. 

Both  layers  of  the  pericardium  are  now  generally  coated 
with  a  thick  layer  of  lymph  ;  and  punctiform  ecchymoses,  or 
in  some  cases  larger  extravasations  of  blood,  are  to  be  seen. 
In  consequence  of  the  movements  of  the  heart  {i.e.  of  the 
opposed  surfaces  of  the  pericardium,  which  are  coated  with 
exudation  matters),  the  exudation  always  presents  a  rough, 
ragged,  or  papillated  appearance.  (See  figs.  141,  142,  143,  144.) 
In  some  cases,  it  is  thrown  into  ridges,  in  others  it  is  honey- 
combed, and  in  many  it  closely  resembles  the  appearance 
which  is  produced  by  forcibly  separating  a  thickly  spread 
sandwich  of  bread  and  butter  ;  in  others,  the  lymph  is  drawn 
out  into  fine  threads  or  strings,  and  the  exterior  of  the  heart 
presents  a  shaggy  appearance — the  so-called  hairy  heart.    (See 

%  143-) 

In  the  earlier  stages  of  acute  cases  the  exudation  materials 
can  be  readily  detached  from  the  surface  of  the  membrane, 
leaving  a  smooth  surface  underneath.     (See  fig.  141.) 

In  some  cases  cancerous  or  tubercular  deposits  (usually 
miliary  tubercles)  are  seen  on  the  surface  of  the  membrane. 
In    these    cases    the    exudation    is    often    haemorrhagic.     In 


302  Diseases  of  t lie  Heart. 

purpura  and  scurvy,  and  in  other  cachectic   conditions,   the 
exudation  also  tends  to  be  bloody. 

In  purulent  pericarditis  the  lymph  is  less  gelatinous, 
more  creamy-looking  and  opaque.  The  exudation  is  generally 
purulent  from  the  first ;  occasionally  a  sero-fibrinous  exuda- 
tion becomes  purulent.  Cachectic  conditions,  pysemia,  puer- 
peral fever,  the  bursting  of  an  abscess  into  the  pericardium, 
etc.,  are  the  conditions  with  which  a  purulent  inflammation  of 
the  pericardium  is  usually  associated. 

After  the  exudation  has  lasted  a  longer  or  shorter  period, 
absorption  and  organisation  occur.  The  fluid  parts  of  the 
exudation  disappear,  the  two  surfaces  of  the  pericardium  come 
in  contact,  and  adhesions  are  usually  developed.  In  some 
cases  the  whole  pericardial  sac  is  obliterated,  frequently  the 
adhesions  are  partial,  occasionally  they  are  limited  to  small 
areas — such  as  the  roots  of  the  great  vessels  or  the  apex.  In 
quite  exceptional  cases  an  example  of  which  has  recently 
came  under  my  observation,  the  inflammatoiy  exudation  is 
absorbed  without  the  formation  of  adhesions.  In  cases  of 
this  description,  limited  opacities  and  thickenings  of  the 
membrane  which  it  is  difficult,  or  impossible  to  distinguish 
from  the  so-called  '  milk-spots,'  which  are  so  frequently  met 
with,  may  be  seen. 

These  so-called  '  milk-spots'  are  most  frequent  over  the 
anterior  surface  of  the  right  ventricle,  at  the  apex,  or  at  some 
other  part  of  the  organ  which  is  exposed  to  friction  and  pres- 
sure. They  are  much  more  common,  therefore,  in  large 
dilated  or  hypertrophied  hearts  {i.e.  in  those  cases  in  which 
the  lungs  acting  as  it  were  as  buffers  or  water  cushions,  arc 
pushed  aside,  and  the  enlarged  heart  comes  in  contact  with 
the  chest  wall).  They  consist  of  localised  thickenings  of  the 
superficial  layers  of  the  pericardium.  (See  fig.  234.)  The}' 
are  undoubtedly  due  to  the  long  continued  irritation  which 
is  produced  by  intermittent  pressure. 

Very  exceptionally  calcareous  salts  are  deposited  when 
the  exudation  matters  are  absorbed  ;  and  in  a  few  cases,  a 
large  portion  of  the  heart  has  been  surrounded  with  a  dense 
calcareous  covering.     This  result  is  more  likely  to  occur  after 


PatJiology  of  Acute  Pericarditis.  303 

purulent  than  after  simple  {i.e.  non-purulent)  pericarditis. 
Calcareous  plates  and  deposits  would  probably  be  more 
frequent  if  it  were  not  for  the  facts,  firstly,  that  purulent 
pericarditis  is  rare,  and,  secondly,  that  the  great  majority  of 
cases  terminate  fatally  during  the  stage  of  suppuration,  i.e. 
before  calcareous  changes  in  the  exudation  matters  can 
occur. 

The  microscopical  appearances  of  pericarditis. — Before  de- 
scribing the  appearances  which  are  seen  under  the  microscope 
in  pericarditis  it  will  perhaps  be  well  to  direct  attention  to  the 
normal  histology  of  the  membrane. 

A  section  through  the  visceral  layer  of  the  pericardium 
and  of  the  cardiac  wall  which  is  situated  beneath  it  (see  fig. 
145)  is  composed  of  the  following  parts  : — 

(i.)  TJie  epitJiclial  layer,  which  consists  of  a  single  layer  of 
pavement  epithelial  cells. 

(2.)   TJie  fibrous  layer,  which  is  composed  of  fibrous  tissue. 

Immediately  beneath  the  epithelium  the  fibres,  which  are 
ordinary  connective  tissue  fibres,  are  arranged  parallel  to  the 
surface  ;  in  the  deeper  parts  of  the  fibrous  layer  they  form  a 
net-work,  and  in  this  part  of  the  membrane  elastic  fibres  are 
found. 


h-- 


Fig.  145. — Section  of  a  part  of  the  pericardium  of  the  right  auricle.   (After  Qiiain. ) 
a,  serous  epithelium  in  section  ;  b,  connective  tissue  layer ;  c,  elastic  network  ; 
(/,  sub-serous  areolar  tissue  ;  e,  fat ;  f  section   of  a  blood-vessel ;  g.  a  small  gan- 
glion ;  //,  muscular  fibres  of  the  myocardium  ;  i,  inter-muscular  areolar  tissue. 


304  Diseases  of  I  lie  Heart. 

(3.)  The  sub-serous  layer,  which  consists  of  areolar  tissue 
and  fat  cells,  and  in  which  the  blood-vessels  and  nerves 
(ganglia  and  nerve  trunks)  are  situated. 

The  sub-serous  connective  tissue  is  continuous  with  the 
connective  tissue  which  passes  between  the  muscular  fibres  in 
the  cardiac  wall^a  connection  of  some  importance,  for  it 
explains  the  facility  with  which  inflammation  travels  from  the 
pericardium  to  the  myocardium,  and  even  to  the  endo- 
cardium. 

The  amount  of  fat  varies  considerably  in  different  cases  ; 
in  spare  individuals  it  is  generally  limited  to  the  furrows  which 
contain  the  larger  blood-vessels,  but  in  fat  persons  it  may 
forma  layer— sometimes  of  considerable  thickness — over  the 
whole,  more  particularly  over  the  anterior  surface,  of  the 
organ. 

The  ganglia  are  most  numerous  in  the  neighbourhood  of 
the  large  vessels,  more  especially  in  the  sulci  which  separate 
the  auricles  from  the  ventricles. 

Now  in  the  earliest  stages  of  pericarditis  the  following 
changes  are  found  : — 

(i.)  The  blood-vessels  are  dilated  and  engorged  with 
blood. 

(2.)  An  exudation  of  fibrinous  lymph  is  seen  on  the  sur- 
face of  the  epithelial  layer,  in  the  deeper  parts  of  the  fibrous 
layer,  and  in  the  sub-serous  areolar  tissue.  The  fibrinous 
lymph  on  the  surface  of  the  membrane  is,  even  in  the  earliest 
stages  in  which  we  have  an  opportunity  of  examining  it, 
arranged  in  the  form  of  irregular  projections  of  various  shapes 
and  sizes.  (See  figs.  146  and  147.)  These  projections  consist 
of  amorphous  or  finely  granular  fibrine  in  which  leucocytes 
and  a  few  larger  cellular  elements,  derived  from  the  epithelium, 
can  generally  be  distinguished.  The  inflammatory  exudation 
is  very  loosely  attached  to  the  surface  of  the  pericardium,  and 
is  readily  detached  in  the  process  of  preparation. 

(3.)  Detachment  and  proliferation  of  the  epithelium.  This 
change,  which  is  well  seen  in  fig.  148,  is  sometimes  difficult  to 
make  out  in  sections,  but  cells  of  various  shapes  and  sizes, 
which    are    undoubtedly    derived    from    the    epithelium,    can 


Pathology  of  Acute  Pericarditis.  305 

usually  be  seen  in  the  meshes  of  the  exudation,  and  in  the 
fluid  contents  of  the  pericardial  sac. 

(4.)  An  exudation  of  leucocytes,  and  in  some  cases  of  red 
blood  corpuscles  in  the  lymph  on  the  free  surface  of  the  mem- 
brane, and  in  the  deeper  parts  of  the  fibrous  and  sub-serous 
layers. 

At  the  lieight  of  the  exiidation  the  layer  of  fibrinous  lymph 
on  the  surface  of  the  pericardium  is  much  increased  in  thick- 
ness, and  the  fibrous  and  sub-serous  layers  of  the  pericardium 
are  more  swollen,  the  exudation  corpuscles  being-  proportion- 
ately more  numerous.  After  a  little  time  new  blood  vessels 
are  formed,  often  in  great  abundance,  in  the  thickened  fibrous 
layer  ;  and  the  rupture  of  these  delicate  vessels  may  be  the 
source  of  the  haemorrhagic  extravasations  which  are  so  fre- 
quently seen  in  the  inflamed  membrane. 

In  a  considerable  proportion  of  cases  the  myocardium  is 
implicated.  The  muscular  fibres,  which  are  situated  imme- 
diately beneath  the  sub-serous  layer,  are  very  generally  affected 
— and  this  is  more  especially  the  case  where  the  inflammation 
is  severe  and  has  lasted  for  any  time.  The  muscular  fibres 
are  swollen  ;  their  transverse  striae  are  indistinct ;  they  stain 
badly  with  picro-carmine  ;  and  in  some  cases  they  are 
distinctly  fatty.  Fibrinous  lymph,  leucocytes,  and  (in  many 
cases)  red  blood  corpuscles  are  seen  amongst  the  areolar 
fibres  and  around  the  fat  cells,  which  pass  from  the  deeper 
surface  of  the  pericardium  into  the  myocardium,  and  in  the 
spaces  which  separate  the  individual  fibres.^ 

In  the  stage  of  absorption  and  resolution  the  fluid  parts  of 
the  exudation  are  removed  by  absorption,  the  exudation 
products  undergo  fatty  degeneration,  and  numerous  fine  oil 
globules  are  seen  in  the  affected  part ;  many  of  the  cor- 
puscular elements  in  the  thickened  fibrous  and  sub-serous 
layers  are  developed  into  spindle  cells,  and  ultimately  into 
fibrous  tissue.  Blood  vessels  shoot  out  from  the  surface  of 
the  membrane  into  the  substance  of  the  exudation  ;  and 
adhesions,   composed   of  spindle   cells   and   fibres,  containing 

'  The  fatty  changes  in  the  muscular  fibres  are  not  generally  observed  unless 
the  inflammation  has  lasted  some  little  time. 


3o6  D/sfczscs  of  the  Heart. 

blood  vessels,  and  in  some  cases  covered  by  a  beautiful  layer 
of  epithelium,  are  formed  between  the  two  opposed  surfaces 
of  the  sac.  In  this  way  the  pericardium  may  be  ultimately 
divided  into  a  large  number  of  secondary  sacs  all  lined  with 
epithelium. 

In  those  cases  in  which  the  adhesions  are  universal,  the  sac 
of  the  pericardium  is  completely  obliterated.  A  thick,  dense, 
fibrous  layer,  consisting  of  spindle  cells,  fibres,  and  containing 
numerous  blood  vessels,  is  in  many  of  these  cases,  found  on 
the  surface  of  the  heart.  The  microscopical  appearances  which 
pericardial  adhesions  present,  are  shown  in  figs.  149  to  157. 

When  the  myocardium  is  at  the  same  time  implicated, 
fibrous  tissue  may  be  formed  in  considerable  quantity  between 
the  muscular  fibres,  which  undergo  fatty  degeneration  and 
atrophy  ;  but  these  changes,  which  are  of  the  greatest  practical 
importance  from  a  clinical  point  of  view,  and  the  secondary 
changes  in  the  heart  which  result  from  adhesions  of  the  peri- 
cardium, will  be  more  appropriately  considered  afterwards. 

The  fibrous  layer  of  the  parietal  pericardium  is  much  less 
frequently  implicated  in  pericarditis  than  the  fibrous  layer  of 
the  portion  of  the  membrane  which  covers  the  heart ;  but  in 
some  cases  the  inflammation  not  only  involves  the  whole 
thickness  of  the  parietal  pericardium,  but  also  extends  to  the 
adjacent  structures — the  pleura,  the  cellular  tissue  of  the 
mediastinum,  or  even  the  lung  itself. 

Tiic  Clinicat  History  of  Acute  Pericarditis. 

In  describing  the  clinical  history  of  acute  pericarditis, 
it  will  be  convenient  to  consider,  in  the  first  place,  the 
individual  symptoms  and  physical  signs,  and  then  to  give  a 
brief  general  description  of  the  chief  types  of  the  affection. 

Syniptovis. — In  order  to  understand  the  symptoms  of 
acute  pericarditis,  it  is  important  to  remember  that,  in  a  large 
proportion  of  cases  the  pericardial  inflammation  is  secondary  ; 
and  that,  in  cases  of  this  description,  the  symptoms  of  the 
primary  disease  are  often  very  striking — so  prominent,  in- 
deed, as  to  obscure  those  which  result  from  the  inflammation 
of  the  pericardium  itself 


Fig.  146. — Section  throtujli  the  wall  of  tJie  left  ventricle  in  early  pericarditis  showing  small  papi/lx  of 
lymph  on  the  surface  of  the  ptricardium.     (^Magnified  about  10  diametersJ) 

e,  endocardium ;  m,  myocardium ;  p,  p,  pericardium  ;  I,  I' ,  lymph. 


^'^m 


Fig.  147. — A  portion  of  (he  same  preparation  more  highly  magnifed  (jibovt  60  diameters). 

TO,  muscular  fibres  of  the  myocardium;  p,  pericardium;  a,  the  papilla  of  IjTiipb  to  which  the 
letter  I'  iu  figure  146  points. 

Note. — To  be  seen  properly  this  figure  should  be  held  about  four  inches  from  the  eye. 

B.  Dei    AD  hat"  tT  LiTMOt  M'LaSAH  JCuMM(t*C  LthO?,  Edu 


a:         gi 


•s.   a 


'^ 


0^~B^ 


•S 

en 

i 

I 

"S 

'"1. 

•<> 

s> 

\!->a 


•Sa     'S 


I" 


Fig.  150. — A  portion  of  the  preiinruui.n  .'i/'wn  in  Jig.  149  more  hirildy  magnijied,  about 
250  diameters,  showing  the  juriction  of  the  fpindlt  ccUed  tisxite,  and  the  li/mph  layer. 
Large  masses  of  lymph  (/,  /,)  are  Lecomiug  converted  into  spindle  cells  («,  s.) 


Fig.  151. 


Fig.  152.- 


----"s-iiV'  ^  /  -<:- 


.XS 


■^1 


^^ 


m^"^. 


Fig.  1 51. — A  portion  of  the  central  lymph  layer  of  trie  preparation  shovm  in  fg.  149, 
magnified  about  200  diameters,  showing  lymph  thi-eads  (a),  leucocytes  (6),  and 
large  epithelial  cells  (c). 


Fig.  152. — Another  portion  of  the  central  lymph  layer  of  the  preparation  shown  in 
fig.  149;  showing  collections  of  red  blood  corpuscles  (o),  surrounded  by 
lymph  threads  (6). 


M°L>u>JCii.>tNcljT> 


Fig.  153. — A  portion  of  tlie  spindle-celled  layer  from  the  section  represented  in  fig.  149,  more  hiyhly 

magnified  (about  250  diameters'). 

a,  spindle  cell ;  b,  capillary  vessel ;  c,  leucocyte. 


Fig.  154. — A  porlion  of  the  preparation  shown  in  fig.  149,  at  the  junction  of  the  mjiocardium  and 
Kpindle-ceUid  layer,  magnifie.il  about  SOO  diameters;  showing  leucocytes  between  the  muscular 
fibres,  proliferation  of  the  nuclei  of  the  muscular  fibres  and  disappearance  of  their  fibrillx. 

s,  spindle  cells;    v,  vessel  transversely  divided;    m,  m,  proliferating  nuclei  of  the  muscular 
fibres  ;  /,  leucocytes  between  the  muscular  fibres. 


M=UiaNlCuM«i«s,ljTnoUoi 


WW 


Fig.  Ibb.— Section  through  a  portion  of  adhererti pericardium  of  old  Uandinn  maonified 
about  £50  diameters.  ^  ^ 

.  a,  a  portion  of  the  parietal  pericardium ;  b.  b,  delicate  connective  tissue  bundles 
passing  between  the  parietal  pericardium  (a)  and  the  \nsceral  pericardium  which  is 
not  shown  in  the  figure ;  c,  c,  nuclei  of  connective  tissue ;  d,  d,  collections  of 
epithelial  cells ;  e,  e,  blood-vessels.  '     »     >  " 


M°|ju>i<Cu»iiii3  bnc*  Eoi. 


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Fig.  157. — Section  Virough  the  thickened  pericardium,  the  result  of  old  pericarditis,  nutgnified  about  180 

diameters. 

The  superficial  parts  of  the  pericardium  contain  nuijierous  spindle  cells  arranged  parallel  to 
the  surface,  which  is  covered  with  a  beautiful  layer  of  epithelium,  much  rounder  in  shape  and  more 
distinct  than  that  covering  the  healthy  pericardium. 

p,  surface  of  pericardium  from  which  the  epithelium  has  become  detached ;  e,  epitheliimi ;  /,  leu- 
cocytes lying  in  a  depression  on  the  surface:  .t,  spindle  cells;  I',  leucocytes  below  the  layer  of 
spindle  cells ;  b,  b,  large  vessels ;  m,  muscular  fibres  of  the  heart. 


M'LxolCuKxm&Lirnc^  Epn* 


Symptoms  oj  Acute  Pericarditis.  307 

In  secondary  cases  of  pericarditis  therefore,  the  cHnical 
picture  is  made  up,  or,  more  correctly,  it  may  be  made  up  (for 
as  we  shall  presently  see,  the  symptoms  due  to  the  inflammation 
of  the  pericardium  itself  are  sometimes  entirely  absent)  of. — 

A.  Symptoms  due  to  the  primary  disease. 

B.  Symptoms  due  to  the  pericardial  inflammation  itself, 
viz. : — 

(i.)  General  symptoms  due  to  the  pericardial  inflamma- 
tion, such  as  fever. 

(2.)  Cardiac  symptoms  proper.  Under  this  head  we  have 
to  consider: — 

{ai)  The  'subjective  cardiac  sensations,'  or  the  symptoms 
which  result  from  the  derangement  of  the  heart  as  a  sensitive, 
vital  organ. 

(^.)  The  symptoms  which  may  result  from  the  derange- 
ment of  the  cardiac  pump — the  mechanical  symptoms,  as  I 
am  in  the  habit  of  terming  them. 

{ci)  The  symptoms,  which  sometimes  result  from  the 
pressure  of  the  enlarged  (distended)  pericardial  sac  upon  sur- 
rounding parts  {i.e.  pressure  symptoms). 

{d.)  Accidental  symptoms  due  to  complications,  or  to  the 
extension  of  the  inflammatory  process  to  adjacent  parts. 

Syjnptoms  due  to  tJie  primary  disease. — It  would  be  out  of 
place  here  to  describe  in  detail  the  symptoms  which  charac- 
terise the  many  different  diseases  with  which  inflammation 
of  the  pericardium  may  be  associated.  I  must,  however, 
emphasise  the  importance  of  looking  out  for  the  symptoms, 
and  more  especially  for  the  physical  signs  of  pericarditis,  in 
all  of  those  diseases,  such  as  acute  rheumatism,  Bright's 
disease,  etc.,  in  which  we  know  that  inflammation  of  the 
pericardium  is  apt  to  occur.  A  trivial  pain  over  the  prse- 
cordium,  for  instance,  which  under  ordinary  circumstances, 
and  in  many  diseased  conditions,  might  be  almost  ignored, 
should,  in  a  case  of  acute  rheumatism  or  Bright's  disease, 
excite  grave  apprehension,  and  necessitate  minute  and  careful 
examination  of  the  heart.  And  this  statement  is  all  the  more 
necessary  because  of  the  fact,  that  the  symptoms  due  to  the 


^^ 


o8  Diseases  of  the  Heart. 

primary  disease  (notably  so  in  acute  rheumatism)  are  often 
very  striking,  and  are  apt  to  overshadow  and  obscure  the 
symptoms,  due  to  the  inflammation  of  the  pericardium — 
symptoms  which  arc  in  many  cases  sHght. 

Syniptojiis  due  to  tlie  pericardial  inflaniuiation  itself. — The 
nature  and  gravity  of  the  symptoms,  which  depend  upon  the 
inflammation  of  the  pericardium  itself,  depend  upon  the 
following  conditions  : — 

(i.)  The  extent  and  severity  of  the  inflammation. 

(2.)  The  condition  of  the  cardiac  muscle,  and  of  the  val- 
vular apparatus  of  the  heart. 

(3.)  The  amount  and  character  of  the  effusion. 

(4.)  The  constitutional  temperament  (susceptibility),  and 
the  previous  state  of  health  of  the  patient. 

(5.)  The  manner  and  degree  in  which  the  cardiac  nerves 
and  ganglia,  on  the  surface  of  the  heart  and  around  the  root  of 
the  aorta,  are  affected  by  the  inflammatory  process. 

In  those  cases  in  which  the  inflammation  is  not  very 
severe;  in  which  the  cardiac  muscle  is  not  implicated;  in  which 
the  amount  of  effusion  is  small ;  in  which  the  patient  was  in 
fair  health  previous  to  the  attack  ;  and  in  which  he  is  not  of 
an  unduly  susceptible  temperament,  the  symptoms  may  be 
extremely  slight  or  altogether  absent.  Indeed,  from  the 
frequency  with  which  we  find  pericardial  thickenings  and 
localised  adhesions  after  death,  it  is  probable  that  many  cases 
of  this  description  pass  entirely  unnoticed.  The  case,  which 
I  have  narrated  on  page  298,  shows  that  even  in  severe  and 
fatal  cases  of  pericarditis,  the  symptoms  may  be  very  slight. 

General  syviptoins  due  to  tlic  pericardial  inflammation — fever. 
— The  fever  is,  as  a  rule,  slight  or  moderate,  and  presents  no 
characteristic  features.  The  tongue,  bowels,  and  urine  pre- 
sent the  usual  alterations  which  are  met  with  in  fever.  When 
the  pericarditis  occurs  in  the  course  of  a  febrile  disease,  such 
as  acute  rheumatism,  the  increase  of  fever  due  to  the  inflam- 
mation of  the  pericardium  is  seldom  sufficiently  great  to 
arrest  attention.  In  purulent  pericarditis  the  fever  may  be 
high,  and  present  the  irregular  ups  and  downs  which,  when 


■  Syiupionis  of  Acute  Pericarditis.  309 

associated  with  rigors  and  sweatings,  are  so  characteristic  of 
suppuration.  When  the  inflammation  extends  to  the  pleura, 
and  more  especially  to  the  lung  itself,  the  fever  is  proportion- 
ately increased.  In  some  cases  there  is  hyperpyrexia,^  and  in 
these  cases  grave  cerebral  symptoms,  the  exact  nature  of 
which  I  shall  presently  describe,  are  usually  developed. 

The  frequency  of  the  pulse  is,  as  a  rule,  considerably 
increased,  the  amount  of  increase  in  the  earlier  stages  being 
proportionate  to  the  amount  of  fever.  In  exceptional  cases 
the  pulse  may  be  slower  than  normal.  In  the  earlier  stages 
it  is  sometimes  full  and  bounding,  and  of  high  tension,  but 
more  frequently  irritable  and  soft.  In  all  cases  of  peri- 
carditis there  is  a  tendency  to  failure  of  the  pulse  and  to  the 
production  of  dicrotism  ;  and  this  is  more  especially  the  case 
where  the  myocardium  is  implicated.  When  endocarditis 
and  valvular  complications  are  present,  the  characters  of  the 
pulse  may,  of  course,  be  profoundly  modified,  the  exact 
characters  depending  upon  the  nature  of  the  valvular  com- 
plication. 

Cardiac  symptoms  proper. — Subjective  cardiac  sensations, 
which  result  from  derangement  of  the.  heart  as  a  vital,  sensi- 
tive organ,  such  as  pain  in  the  region  of  the  heart,  a  feeling 
of  tightness  or  constriction  about  the  chest,  and  (occasionally) 
palpitation  or  intermittent  action  of  the  heart,  are  experienced 
in  the  great  majority  of  cases  of  pericarditis. 

Cardiac  symptoms  of  this  description  are  suggestive  of 
the  presence  of  pericarditis,  but  they  are  not  distinctive  of 
that  condition.  In  short,  the  student  should  distinctly 
understand  that  the  symptoms  of  pericarditis  {i.e.  the  symp- 
toms as  distinct  from  the  physical  signs)  are  by  no  means 
characteristic. 

According  to  Sibson's  elaborate  statistics,  pain  of  a  more 
or  less  continuous  character  is  present  in  three-fourths  of  the 

'  The  exact  cause  of  the  hyperpyrexia  is  not  known.  It  is  much  more  common 
in  cases  of  rheumatic  fever,  complicated  with  pericarditis,  than  in  cases  which 
are  unattended  with  that  condition.  The  statistics  of  the  Clinical  Society  of 
London  seem  to  show  that  the  pyrexia  is  not  associated  so  frequently,  as  was 
formerly  supposed,  with  suppression  of  perspiration. 


3IO  Diseases  of  tJic  Heart. 

cases  of  rheumatic  pericarditis.  It  is  most  marked  in  cases 
of  '  dry'  pericarditis,  and  usually  disappears  when  the  effusion 
becomes  copious.  Its  intensity  is  not  as  a  rule  great,  but  in 
some  cases  '  the  suffering  and  distress  over  the  heart  are  so 
great  as  to  drown  all  other  complaints.'  In  a  considerable 
proportion  of  cases  there  is  pain  and  tenderness  in  the  pit  of 
the  epigastrium  ;  and  in  some  cases  there  is  also  tenderness 
on  pressure  over  the  region  of  the  heart  itself^ 

In  exceptional  cases  a  constrictive  pain  in  the  chest, 
radiating  to  the  left  shoulder  and  down  the  left  arm,  and 
resembling  the  pain  of  angina  pectoris,  is  met  with.  It  pro- 
bably depends  upon  the  fact  that  the  cardiac  nerves  (branches 
of  the  cardiac  or  coronary  plexuses)  are  irritated  by  the 
inflammatory  process. 

One  of  the  most  marked  cases  of  angina  pectoris  which  I 
have  ever  seen,  was  attended  with,  and  apparently  depended 
upon  pericarditis.     The  following  is  an  abstract  of  it : — 

Case — Angifia  pectoris;  perica?'difis  of  obscure  origin. 

The  patient  was  a  ship-captain,  iist.  49,  of  a  florid  complexion  and 
sanguine  temperament.  He  had  suffered  from  syphilis,  and  had  perhaps 
indulged  somewhat  too  freely  in  alcohol,  but  had  been  in  vigorous 
health  up  to  the  occurrence  of  the  attack.  The  pain  commenced  gradu- 
ally in  the  region  of  the  heart,  and  continued  more  or  less  constantly  for 
a  fortnight.  It  was  severe  throughout  the  attack,  and  was,  as  a  general 
rule,  confined  to  the  region  of  the  heart ;  ever)'  now  and  again — some 
days  several  times  in  the  twenty-four  hours — it  became  greatly  intensified, 
and  assumed  the  characteristic  features  of  angina  pectoris.  During  the 
earlier  days  of  the  attack  nothing  of  importance  was  detected  in  the 
condition  of  the  heart,  but  well  marked  pericardial  friction  subsequently 
developed.     At  the  end  of  a  fortnight  the   pain   and  pericardial  friction 


'  Sibson  concludes,  probably  with  truth,  '  that  the  pain  on  pressure  below  or 
at  the  side  of  the  ensiform  cartilage  is  in  these  cases  due,  not  to  peritonitis,  but 
to  inflammation  of  the  fibrous  structure  and  pericardial  or  inner  surface  of  the 
central  tendon  of  the  diaphragm,  where  it  forms  the  floor  of  the  pericardial 
sac,  and  the  lower  and  anterior  portion  of  that  sac'  The  same  authority  states, 
'  that  if  the  pain  over  the  heart  is  increased  or  excited  by  pressure  over  the 
region  of  the  organ,  it  may,  with  an  approach  to  certainty,  be  attributed  to 
nflammation  of  the  pleura,  especially  if  the  pain  on  pressure  is  complained  of, 
not  before,  but  at  the  time  of  or  after  the  first  presence  of  the  friction  sound.' — 
Russell  Reynold's  System  of  Medicine^  vol.  iv.  pp.  230  and  224. 


Symptoms  of  Acute  Pericarditis.  31 1 

both  disappeared,  and  the  patient  apparently  made  a  complete  recover)-. 
I  am  unacquainted  with  the  after  progress  of  the  case,  and  I  ha^•e 
never  been  quite  able  to  satisfy  myself  as  to  the  exact  cause  of  the  attack. 
The  aortic  second  sound  was  throughout  the  attack,  and  also  subsequent!)-, 
somewhat  accentuated,  and  I  have  often  surmised  that  the  cause  of  the 
pericarditis  was  the  pressure  of  an  aneurism  originating  immediately 
above  the  sigmoid  valves. 

Mechanical  symptoms,  which  result  from  disturbance  of  the 
action  of  the  cardiac  pump  (such  as  pallor  or  lividity  of  the 
countenance,  irregularity  and  failure  of  the  heart's  action,  the 
pulsus  paradoxicus,  faintness,  difficulty  of  breathing,  ortho- 
pnoea,  etc.)  are  usually  observed  in  severe  cases.  They  may 
be  due  to  one  or  other  of  the  following  conditions  : — 

{a)  Effusion  into  the  sac  of  the  pericardium  sufficiently 
copious  to  embarrass  the  action  of  the  heart,  and  to  interfere 
with  the  course  of  the  circulation.  A  large  effusion,  more 
especially  if  it  is  rapidly  poured  out,  may  seriously  interfere 
with  the  course  of  the  ciixulation,  by  compressing  the  thin- 
walled  auricles,  the  venae  cavae,  and  pulmonary  veins,  and  so 
prevent  the  due  supply  of  blood  to  the  aorta  and  pulmonary 
artery.  The  right  auricle  and  superior  cava,  iti  consequence 
of  the  comparative  thinness  of  their  walls,  are  affected  most 
by  the  pressure.  In  consequence  of  the  pressure  on  the 
superior  cava,  the  veins  in  the  neck  become  distended,  and 
the  greater  the  pressure  on  the  superior  cava  the  greater  the 
distention  of  the  veins.  In  cases  of  pericarditis,  fulness 
of  the  veins  of  the  neck  is,  therefore,  suggestive  of  co- 
pious effusion,  more  especially  when  there  is  no  evidence  of 
endocarditis  or  over-distention  of  the  right  cavities  of  the 
heart. 

{bi)  Inflammation  of  the  cardiac  muscle. 

ici)  Endocarditis  and  associated  valvular  lesions. 

Mechanical  symptoms  are  only  seen  in  severe  cases 
of  pericarditis  (cases  with  copious  effusion),  or  in  those  cases 
in  which  the  inflammation  of  the  pericardium  is  associated 
with  disease  of  the  muscular  walls  or  valvular  mechanism  of 
the  heart.  In  fact,  in  any  case  of  pericarditis  in  which 
mechanical  symptoms  were  prominent,  we  would  probably  be 


3 1 2  Diseases  of  tJie  Heart. 

correct  in  concluding  that  there  was  something  more  than 
mere  inflammation  of  the  pericardium  present  {i.e.  that  either 
myocarditis  or  endocarchtis  was  present.) 

Pressure  symptoms. — When  the  effusion  is  very  extensive, 
the  greatly  distended  pericardial  sac  may  press  upon  the 
oesophagus  and  produce  difficulty  in  swallowing  (dysphagia), 
or  upon  the  trachea  or  left  bronchus,  and  cause  cough  and 
difficulty  in  breathing.  These  symptoms  are  aggravated  by 
the  recumbent,  and  relieved  by  the  sitting  posture. 

Aeeidcntal  symptoms,  due  to  the  extension  of  the  inflam- 
ination  to  surrounding  parts  (other  than  the  myocardium  or 
endocardium),  or  to  the  presence  of  complications,  are  of 
common  occurrence.  In  a  considerable  proportion  of  cases, 
pleurisy,  with  its  attendant  symptoms  and  signs  (pain  in  the 
side,  etc)  develops.  In  a  few  cases,  pneumonia  or  pulmonary 
apoplexy  is  met  with.^  In  rare  cases,  more  especially  in 
rheumatic  pericarditis,  cerebral  symptoms  and  hyperpyrexia 
occur.  Hyperpyrexia  is,  according  to  the  elaborate  report  of 
the  Clinical  Society  of  London,  much  more  frequent  in  males 
than  in  females,  and  is  much  more  common  in  a  first  than  in 
subsequent  attacks  of  rheumatic  fever.  The  nervous  symp- 
toms met  with  in  connection  with  it  are  in  the  order  of  their 
relative  frequency  as  follows : — *  delirium  (in  all  phases), 
insomnia,  restlessness,  muscular  tremors,  involuntary  dis- 
charges, subsultus  tendinum,  coma  (a  late  symptom),  head- 
ache, tremor  of  tongue,  deafness,  tonic  spasms  (in  two  cases 
of  tetaniform  character),  risus  sardonicus,  convulsions,  flocci- 
tation,  tinnitus  aurium,  giddiness,  drowsiness,  vomiting,  silli- 
ness of  manner,  fearfulncss,  hesitating  speech,  chorea,  hyper- 
jEsthesia.'  'The  delirium,  which  is  the  most  frequent  symp- 
tom met  with  in  these  cases,  sometimes  precedes,  sometimes 

'  Pleuritic  pain  was  present  in  one  half  of  Sibson's  cases  of  rheumatic  peri- 
carditis. He  says  that  it  may  Ije  due  to  two  causes,  viz.: — one,  the  extension  of 
the  inflammation  through  the  fibrous  structure  of  the  pericardium  to  the  pleura 
covering  it ;  the  other,  the  occurrence  of  pulmonary  apoplexy  with  its  attendant 
pleurisy. — Russell  Reynolds,  vol.  iv.  p.  233. 


Syiuptonis  of  Acute  Pericarditis 


0^6 


accompanies,  and  sometimes  follows  the  onset  of  the  hyper- 
pyrexia.' One  half  of  the  cases  of  hyperpyrexia,  collected  by 
the  Clinical  Society,  terminated  fatally.  The  duration,  after 
the  development  of  the  nervous  symptoms,  varies  from  a  few 
hours  to  three,  four,  or  five  days. 

In  addition  to  the  delirium  which  is  associated  with 
hyperpyrexia,  Sibson,  Austin  Flint,  and  others,  have  described 
a  peculiar  form  of  mental  derangement,  characterised  by  a 
state  of  taciturn  melancholia  and  (according  to  Austin  Flint) 
a  suicidal  tendency.  According  to  Sibson's  observations,  the 
cases  of  pericarditis,  in  which  this  peculiar  form  of  mental 
aberration  was  met  with,  were  almost  always  complicated 
with  endocarditis,  and  in  some  cases  chorea  subsequently 
developed  ;  and  Sibson  suggests  that  the  condition  is  due  to 
embolic  plugging  of  minute  vessels  of  the  cerebral  cortex. 
This  form  of  delirium  differs  from  the  delirium  which  is 
associated  with  hyperpyrexia,  in  as  much  as  it  is  not  associ- 
ated with  fever,  its  duration  is  much  longer  (from  three  weeks 
to  three  months,  according  to  Sibson),  and  in  the  fact  that 
the  majority  of  cases,  which  are  not  complicated  with  chorea, 
terminate  in  recovery. 

In  a  third  group  of  cases  of  pericarditis,  a  form  of  delirium 
which  resembles  more  or  less  closely  delirium  tremens,  is 
met  with.  This  form  is,  according  to  Sibson,  usually  asso- 
ciated with  moderate  fever,  and  occurs  in  persons  of  an 
anxious  nervous  disposition,  in  those  who  have  been  addicted 
to  alcoholic  excess,  or  who  have  been  exposed  to  want  and  pri- 
vation.   It  is  sometimes  seen  in  connection  with  hyperpyrexia. 

/;/  addition  to  tJic  syiuptonis  already  ennnierated,  the 
following  may  be  added  : — 

Alteration  of  the  eountenanee. — In  a  large  proportion  of 
cases  the  facial  physiognomy  is  altered.  In  some  the  face 
is  flushed.^  This  condition  is  seen  more  especially  in  the 
earlier  stages  of  rheumatic   cases   {i.e.  in  cases  in  which  the 

'  Sibson  suggests  that  flushing  and  pallor  of  the  countenance  may  in  some 
cases  be  due  to  reflex  disturbance  of  the  vaso-motor  centre,  the  pericardial  inflam- 
mation acting  as  the  peripheral  source  of  irritation. 


314  Diseases  of  tJie  Heart. 

action  of  the  cardiac  pump  is  not  as  yet  embarrassed),  and  is 
generally  associated  with  profuse  sweating. 

In  others,  the  face  is  pale,  pinched,  and  anxious;  and  there 
may  be  other  indications  of  collapse  and  nervous  exhaustion, 
such  as  nausea,  vomiting,  restlessness,  insomnia,  a  weak 
thready  or  irregular  pulse,  etc.  Severe  pain  in  the  region  of 
the  heart  or  in  the  joints,  and  sudden  failure  of  the  heart's 
action,  as  the  result  of  copious  effusion,  myocarditis,  valvular 
complications,  etc.,  are  the  most  frequent  causes  of  this  state 
of  depression. 

In  others,  again,  the  countenance  is  more  or  less  dusky, 
livid,  or  congested.  This  condition  is  generally  seen  in  the 
later  stages  of  the  case,  and  is  associated  with  obstructed 
venous  return,  the  causes  of  which  I  have  already  described 
in  speaking  of  the  mechanical  symptoms.     (See  p.  311.) 

Cough,  hoarseness,  and  aphonia. — A  short,  dry,  irritable 
cough  is  often  present,  and  in  some  cases  there  is  hoarseness 
or  aphonia.  The  latter  symptoms  probably  depend  upon 
irritation  of  the  left  recurrent  laryngeal  nerve  as  it  winds 
round  the  root  of  the  aorta. ^ 

Physical  signs. — The  physical  condition  of  the  pericardium 
is  ascertained  by  the  same  means  by  which  we  ascertain  the 
condition  of  the  heart  itself,  and  it  is  important  to  remember 
that,  under  normal  circumstances,  the  opposed  surfaces  of  the 
sac  are  in  close  contact,  and  move  smoothly  and  noiselessly 
one  upon  the  other,  and  that  the  signs  derived  from  the 
physical  examination  of  the  pericardium  are  entirely  negative. 
In  other  words,  the  size  and  shape  of  the  pericardium  corre- 
spond, in  conditions  of  health,  exactly  to  the  size  and  shape  of 
the  heart  itself,  and  the  outlines  of  the  two  structures  cannot 
be  distinguished  by  means  of  percussion,  while  on  listening 
over  the  pericardium  the  sounds  of  the  heart  are  alone  heard.- 

'  In  a  case  observed  by  Baeumler  (quoted  by  Bauer,  Zienissen's  Cyclopaedia, 
vol.  vi.  p.  603),  double  paralysis  of  the  vocal  cords,  due  to  the  pressure  of  a  large 
pericardial  effusion  upon  both  recurrent  nerves,  was  observed. 

*  It  has  been  stated  that,  during  violent  action  of  the  heart,  a  friction  sound 
is  sometimes  produced  within  the  normal  pericardium,  but  in  common  with  other 
observers  I  am  disposed  to  doubt  the  statement. 


Phydcal  signs  of  Acute  Pericarditis.  3 1 5 

Now  in  pericarditis  the  physical  conditions  are  entirely 
altered,  and  it  is  only  by  keeping  the  nature  of  the  altera- 
tions prominently  in  view,  that  it  is  possible  to  understand  in- 
telligently the  alterations  in  the  physical  signs  which  occur 
when  the  membrane  is  inflamed.  These  alterations  are  as 
follows  : — 

Firstly,  the  surfaces  of  the  pericardium  become  covered 
with  a  layer  of  lymph,  and  the  rubbing  together  of  the  two 
opposed  rough  and  inflamed  surfaces  {i.e.  of  the  visceral  and 
parietal  layers  of  the  sac),  which  occurs  during  the  systolic 
and  diastolic  movements  of  the  heart,  is  attended  with  the 
production  of  vibrations,  w^iich  are  heard,  through  the  stetho- 
scope as  friction-sounds  or  murmurs,  and  can,  in  some 
instances,  be  felt  by  the  hand  placed  over  the  prsecordium  as 
friction  fremitus. 

Pericardial  friction-sounds  and  pericardial  friction  fremitus 
may  be  termed  tlie  pJiysical  signs  zuliic/t  result  from  roughening 
of  the  membrane. 

Secondly,  fluid  is  poured  out  into  the  interior  of  the  sac. 
In  many  cases  the  distention  of  the  sac  is  sufficiently  great — 

{ci)  To  give  rise  to  increased  dulness  on  percussion  over  the 
praecordium,  and  to  enable  us,  in  some  cases,  to  differentiate, 
by  means  of  percussion,  the  outline  of  the  pericardium  from 
the  outline  of  the  heart. 

(/;)  To  produce  such  displacement  in  the  position  of  the 
heart,  that  the  cardiac  impulse  and  the  apex  beat  are  either 
altered  from  the  normal  position  or  (in  rare  cases)  completely 
effaced — physical  facts  which  we  determine  by  means  of 
palpation. 

((f)  To  cause  lateral  displacement  of  the  lungs,  and  down- 
ward displacement  of  the  diaphragm  and  therefore  of  the  left 
lobe  of  the  liver. 

id)  To  cause,  more  especially  where  the  effusion  is  con- 
siderable and  the  chest  wall  elastic,  bulging  of  the  praecordium 
and  widening  of  the  intercostal  spaces  corresponding  to  this 
part  of  the  chest. 

ie)  By  compressing  the  auricles  and  veins,  to  cause  disten- 
tion of  the  veins  of  the  neck,  and  to  interfere  with  the  natural 


J 


1 6  Diseases  of  tJic  Heart. 


course  of  the  circulation — effects  which  I  have  already  alluded 
to,  and  which  are  of  course  manifested  by  distinct  symptoms 
and  physical  signs. 

The  physical  signs  which  are  due  to  the  conditions  enumer- 
ated under  headings  a,  b,  c,  d,  and  e,  may  be  termed  ihc  physical 
signs  wJiich  result  {or  rather  ivJiicJi  may^  result)  from  effusion 
into  the  sae. 

Now  in  some  cases  the  effusion  is  never  sufficiently  great 
to  produce  increased  dulness  on  percussion,  and  the  other 
physical  signs  which  I  have  termed  '  the  physical  signs  which 
result  from  effusion  into  the  sac'  In  other  cases,  when  the 
patient  first  comes  under  observation,  the  effusion  is  not  as 
yet  sufficiently  extensive  to  alter  the  percussion  outline  of  the 
heart,  although  it  subsequently  may  become  so.  In  others 
again,  although  sufficiently  extensive  to  produce  increased 
dulness  at  an  earlier  period  of  the  case,  it  has  already  been  in 
great  part  absorbed  before  the  patient  comes  under  observa- 
tion. In  all  of  these  cases  the  physical  signs  will  simply  be 
those  which  are  due  to  roughening  of  the  walls  of  the  sac,  in 
short,  those  of  the  so-called  dry"^  form  of  pericarditis. 

In  the  so-called  moist  variety  of  pericarditis,  on  the  con- 
trary, the  physical  signs  are  not  merely  those  which  result 
from  effusion  into  the  sae.  The  pericardial  friction  usually 
continues  throughout  the  period  of  effusion.  Moist  peri- 
carditis is,  therefore,  characterised  by  physical  signs  resulting 
both  from  effusion  into  the  sac  and  roughening  of  the  peri- 
cardial membrane. 

Let  us  now  consider  some  of  the  more  important  of  these 
physical  signs  a  little  more  in  detail. 

Character  of  Pericardial  Friction  Sounds. 

Rhythm. — In  typical  cases  pericardial  friction  is  double,  a 
to-andfro  sound,  as  it  has  been  termed,  the  to  and  fro  corre- 

'  I  say  may  result,  for  unless  the  effusion  is  considerable,  some  of  them  at  all 
events  (distention  of  the  veins  of  the  neck,  for  instance),  are  not  produced. 

^  The  somewhat  artificial  division  into  dry  and  moist,  is  especially  useful  in 
describing  the  physical  signs.  Dry  pericarditis  may  be  defined  as  pericarditis  in 
which  the  amount  of  effusion  is  not  sufficiently  extensive  to  be  detected  by  means 
of  percussion  ;  while  moist  pericarditis  may  be  defined  as  pericarditis  in  which  the 
effusion  is  sufficiently  extensive  to  be  detected  by  means  of  percussion. 


Physical  signs  of  Acute  Po'icardiiis.  3  i  7 

spending  to  the  rubbing  of  the  two  rough  surfaces  of  the 
membrane  during  the  systole  and  the  diastole  of  the  heart  re- 
spectively. The  synchronism  with  the  heart  sounds  is  seldom 
very  exact,  and  in  this  respect  there  is,  as  we  have  previously 
seen,  an  important  distinction  between  pericardial  and  endo- 
cardial murmurs.  The  two  divisions  of  the  sound  are,  as  a 
rule,  of  equal  duration,  the  systolic  portion  being  generally 
louder  than  the  diastolic.  Occasionally  the  pericardial  friction 
sound  is  single,  and  it  is  then  systolic  {i.e.  it  corresponds  rather 
to  the  first  than  to  the  second  sound  of  the  heart).  In  some 
cases  it  is  triple,  and  presents  3.  presystolic  as  well  as  a  systolic 
and  diastolic  rhythm. 

Point  of  inaximuni  intensity  and  direction  of  propagation. — 
Pericardial  friction  is  usually  best  heard  over  that  part  of  the 
heart  which  comes  in  most  direct  and  forcible  contact  with 
the  front  wall  of  the  chest.  Under  ordinary  circumstances, 
therefore,  the  friction  is  first  and  best  heard  over  the  front 
of  the  right  ventricle,  that  is  to  say,  over  the  lower  end  of 
the  sternum  and  the  adjacent  costal  cartilages.  In  many 
cases  the  friction  sound  is  limited  to  the  pra^cordial  region, 
and  very  often  to  the  part  of  the  chest  wall  which  corresponds 
to  the  exact  point  of  the  sac  at  which  the  friction  is  produced ; 
though,  as  Sibson  has  shown,  when  the  vibrations  are  directly 
communicated  to  the  sternum,  as  they  are  most  likely  to  be 
in  cases  of  dry  pericarditis  {i.e.  when  there  is  no  intervening 
layer  of  lung  tissue  or  of  fluid  between  the  point  of  their  pro- 
duction and  the  front  wall  of  the  chest),  the  friction  sound 
may  be  conducted  in  various  directions  by  the  sternum  and 
costal  cartilages,  which  are  attached  to  it — the  sternum  acting 
as  a  sounding  board.  Pericardial  friction  sounds  have  no  de- 
finite and  distinct  lines  of  propagation  as  endocardial  murmurs 
have. 

Sound  Character. — In  the  majority  of  cases  the  sound,  as 
the  i&rva  frietion  murmur  suggests,  is  harsh,  and  gives  one  the 
distinct  impression  of  being  produced  by  the  rubbing  together 
of  two  rough  surfaces.  In  many  cases  it  is  actually  grating 
or  creaking  (resembling  the  sound  produced  by  the  creaking 
of  new  leather  '  bruit  de  cuir  neuf")  ;  exceptionally  it  is  soft  in 


3i8  Diseases  of  t lie  Heart. 

character.  It  is  usually  superficial,  i.e.  it  seems  to  be  pro- 
duced immediately  under  the  ear.  In  addition  to  these 
characters,  which  are  usually  of  themselves  quite  conclusive, 
pericardial  friction  is  almost  invariably  intensified,  and  in 
many  cases  its  sound  characters  are  absolutely  altered  by  the 
pressure  of  the  stethoscope;  the  effect  of  this  pressure  being  of 
course  to  bring  the  two  roughened  surfaces  of  the  pericardium 
in  closer  and  firmer  contact  one  with  the  other.  Pericardial 
friction  sounds,  too,  are  very  apt  to  undergo  spontaneous 
alterations  in  character  (rhythm,  tone,  area,  etc.),  and  this 
is  more  particularly  the  case  in  the  earlier  periods  of  the 
inflammation,  and  depends  of  course  upon  the  fact  that  the 
physical  conditions  within  the  sac  (amount  of  exudation,  etc.), 
are  then  undergoing  rapid  alterations. 

When  the  friction  sound  is  loud,  the  normal  heart  sounds 
are,  as  a  rule,  completely  obscured  by  it ;  when  the  friction 
sound  is  soft  the  normal  heart  sounds  may,  as  it  were,  be 
heard  through  it.  In  those  cases  in  which  endocarditis  and 
valvular  complications  are  present,  valvular  murmurs  are  some- 
times audible  in  addition  to  the  pericardial  friction  sounds. 

The  loudness  and  tone  of  the  pericardial  friction  sound 
seem  to  depend  upon: — (i)  the  force  with  which  the  two 
opposed  surfaces  of  the  roughened  pericardium  are  rubbed 
together,  and  the  amount  of  movement  which  takes  place 
between  them,  that  is  to  say  upon  the  force  with  which  the 
heart  is  contracting,  and  the  amount  of  the  external  resistance 
opposed  to  its  contraction,  which  in  its  turn  depends  upon 
the  position  of  the  organ  in  the  thorax,  and  especially  the 
relationship  of  the  organ  to  the  front  wall  of  the  chest ;  and 
(2)  the  amount  and  consistency  of  the  lymph.  Vigorous 
action  of  the  heart ;  close  contact  of  the  organ  with  the 
front  wall  of  the  chest,  more  especially  of  the  right  ventricle 
with  the  sternum  ;  a  small  amount  of  fluid  in  the  sac  ;  and 
a  thick  layer  of  tolerably  tough  lymph  on  the  two  opposed 
surfaces  of  the  pericardium,  seem  to  be  the  conditions  which 
favour  the  production  of  loud  pericardial  friction  ;  and  other 
things  being  equal,  the  louder  the  friction  sound  the  more 
extensive  the  area  over  which  it  is  propagated. 


Physical  signs  of  Acute  Periccn-ditis.  319 

Dulness  on  Percussion  over  tlie  Prceconiiui/i. 

The  dulness  which  is  due  to  effusion  into  the  sac  of  the 
pericardium  presents  certain  important  characteristics. 

Its  extent  depends  upon  the  amount  of  effusion  into  the 
sac,  the  more  extensive  the  effusion  the  greater  the  dulness. 
The  condition  of  the  anterior  margins  of  the  lungs  is  also  of 
considerable  importance  ;  when  the  lungs  are  very  voluminous, 
as  in  emphysema,  or  when  their  anterior  margins  are  fixed  to 
the  front  wall  of  the  chest  by  adhesions,  the  dulness  is  by 
no  means  so  extensive  as  when  they  are  normal  and  can  be 
readily  pushed  aside  and  compressed  by  the  enlarging  sac. 

The  fonn  and  outline  of  the  dulness  correspond  to  the 
form  and  outline  of  the  pericardial  sac  ;  and  since  the  peri- 
cardium is  not  reflected  at  the  base  of  the  heart,  but  includes 
in  its  narrower,  upper  part  a  considerable  portion  of  the  great 
vessels,  it  follows  that  the  area  of  dulness  which  results  from 
distention  of  the  sac  is  pyramidal  (more  correctly  a  truncated 
pyramid,  the  apex  being  above,  the  base  below)  or  pear- 
shaped — the  stalk  of  the  pear  corresponding  to  the  upper  and 
narrower  part  which  surrounds  the  great  vessels,  the  body  of 
the  pear  to  the  lower  part  of  the  distended  sac  which  surrounds 
the  heart  itself.  The  peculiar  shape  of  the  dulness  is  of  great 
diagnostic  value  ;  and  another  point  which  is  equally  import- 
ant as  an  indication  of  pericardial  effusion,  but  which  unfor- 
tunately is  not  always  present,  is  that  in  some  cases  the  area 
of  dulness  extends  beyond,  i.e.  further  to  the  left  than  the 
apex-beat — z.^.  the  left  apex  beat.  In  figure  158,  the  shape 
of  the  pericardium,  when  artificially  distended  with  fluid,  is 
shown  ;  in  fig.  159,  the  appearance  which  the  sac  may  present 
when  greatly  distended  in  disease.  In  fig.  160,  the  character- 
istic pear-shaped  outline,  which  the  dulness  presents,  is  well 
seen. 

Some  recent  writers  differ  from  the  usually  received  opinion,  that  the 
form  of  the  area  of  cardiac  dulness  is  characteristic  of  pericardial  effusion. 
Thus  Dr  Rotch,  in  the  Supplement  to  Ziemssen's  CyclopcBdia  of  the  Prac- 
tice of  Medicifte,  page  363,  says,  'Bauer's  opinion,  that  the  triangular  shape 
of  the  area  of  dulness  depends  upon  the  shape  of  the  pericardial  sac,  has 
not  been  substantiated  by  later  observations,  the  theory  of  Duchek  having 
been  found  to  be  more  correct,  namely  that  in  cases  uncomplicated  by 


320 


Diseases  of  the  Heart. 


pleuritic  adhesions  it  is  the  retraction  of  the  edges  of  the  lungs  which 
determines  the  shape  of  the  absolutely  dull  area  and  that  therefore  the 
so-called  triangular  figure  can  be  produced  by  an  enlarged  heart  as  well 
as  a  pericardial  effusion.' 


Fig.   158. 


Fig.   159. 


Fic;.  15S. — Pericardium  distended  intojifteen  oiiiiees  ofjiuid.     (After  Sibson.) 
P'lG.  159.  —  Case  of  pericarditis  in  'which  the  sac  contained  3^  ll)s.  of  fluid. 

Altered  Position  of  the  Heart  and  Apex  Beat. 
The  effusion  at  first  collects  at  the  sides  of  the  heart,  at 
the    bottom    of   the    pericardial    sac,   and    around    the    great 


Physical  Signs  of  AciUe  PeTicarditis.         321 


Fig.    160.  —  Outline  of  percussion  dulness  in  a  case  of  pericardial  effusion. 
(After  Sibsoii.) 


vessels.  As  it  becomes  more  and  more  copious  the  sac 
becomes,  of  course,  more  and  more  distended,  and  the  heart 
is  pushed  upwards,  the  apex  being  tilted  towards  the  left. 
In  consequence  of  this  alteration  in  the  position  of  the  heart, 
the  position  of  the  cardiac  impulse  is  altered,  the  lower 
boundary  of  the  impulse  being  situated  in  the  fourth  or  even 
the  third,  instead  of  in  the  fifth  interspace,  as  it  is  in  health. 
The  apex  beat  not  unfrequently  corresponds  to  the  left 
nipple,  and  in  some  cases  it  may  be  situated  slightly  above, 
and  to  the  outer  side  {i.e.  to  the  left)  of  the  nipple.  When 
the  effusion  is  copious,  the  apex  beat  is  usually  impaired  in 
force  or  altogether  effaced.  In  exceptional  cases,  owing  to 
the  fact  that  the  heart  is  enlarged,  as  the  result  of  previous 
disease,  or  tied  down,  as  the  result  of  previous  pericarditic 
adhesions,  the  position  of  the  heart  and  apex  beat  is  not 
altered.  When  the  effusion  is  absorbed,  the  heart  and  with 
it  the  cardiac  impulse  and  apex  beat  usually  return  to  the 
normal    position.      An    exception   to   this,  the  general   rule, 

X 


32  2  Diseases  of  the  Heart. 

occurs  in  some  cases  in  which  adhesions  are  formed  while 
the  heart  is  still  in  its  displaced  position. 

In  consequence  of  the  alteration  in  the  position  of  the 
heart,  which  occurs  in  most  cases  of  copious  effusion,  the 
area  of  the  pericardial  friction  sounds,  which  we  have  previ- 
ously seen  persist,  as  a  rule,  through  the  period  of  effusion, 
is  also  displaced  upwards.  The  to-and-fro  murmur  may, 
therefore,  be  heard  in  the  third  or  fourth  interspaces,  and 
considerably  to  the  left  of  the  sternum  instead  of  over 
the  lower  end  of  the  sternum  and  the  adjacent  lower  left 
costal  cartilages,  as  it  is  in  cases  of '  dry'  pericarditis.  When 
the  fluid  is  absorbed,  and  the  heart  returns  to  its  normal 
position,  the  area  of  friction  moves  downwards  with  it. 

Prominence  or  bulging  of  the  preeeordinni  and  sivelling  in 
the  pit  of  the  epigastrium  are  sometimes  observed  when  the 
effusion  is  copious.  Decided  prominence  of  the  prsecordial 
region  only  occurs  when  the  chest  wall  is  elastic,  and  is 
therefore  most  commonly  seen  in  young  subjects  ;  it  would  be 
more  frequent  in  women  than  in  men  if  it  were  not  usually 
obscured  by  the  prominence  of  the  left  mamma.  The  lower 
left  intercostal  spaces  are  widened,  and  some  observers  have 
described  fluctuation  in  them,  but  this  condition  (fluctuation) 
is  probably  very  rarely  (if  ever)  present,  in  acute  pericarditis. 

General  survey  of  the  symptoms  and pliysical  signs. — Let  us 
now  take  a  brief  general  survey  of  the  symptoms  and  signs 
of  acute  pericarditis  ;  and  remembering  that  acute  inflam- 
mation of  the  pericardium  is  usually  secondary,  let  us  omit 
for  the  purposes  of  description  the  symptoms  which  are  due  to 
the  primary  disease,  and  limit  the  description  to  those  which 
result  from  the  inflammation  of  the  pericardium  itself 

It  will  be  self  evident  from  what  I  have  already  stated, 
that  cases  of  acute  pericarditis  vary  very  considerably  in  the 
severity  of  the  symptoms,  and  in  the  nature  of  the  physical 
signs  which  they  present.  The  following  types  of  the  disease 
may  be  described  : — 

I.  Cases  of  latent  periearditis. — In  these  cases  the  symp- 
toms are  extremely  slight  or  altogether  absent,  and  in   many 


Symptoms  of  Acute  Pericarditis. 


6^6 


cases  of  this  description  the  condition  entirely  escapes  notice. 
The  effusion  is  for  the  most  part  slight,  but  the  case  which 
I  have  related  on  page  298,  shows  that  a  considerable 
effusion  may  be  unattended  by  any  marked  symptoms. 
Latent  pericarditis  very  rarely  indeed  proves  fatal  ;  the  case 
to  which  I  have  just  alluded  shows,  however,  that  death 
does  occasionally  occur  from  syncope. 

2.  Uncomplicated  cases  of  dry  pericarditis  zvJiich  are  at- 
tended by  distinct  symptoms. — In  these  cases  there  are  no 
mechanical  symptoms  ;  pain  in  the  region  of  the  heart  is  the 
chief  complaint ;  the  countenance  may  present  evidence  of 
suffering,  but  the  general  constitutional  symptoms  are  not,  as 
a  rule,  severe.  On  auscultation  the  characteristic  pericardial 
friction  murmur  is  heard  over  the  praecordium  (usually  over 
the  lower  end  of  the  sternum  and  adjacent  costal  cartilages, 
though  in  some  cases  it  is  much  more  diffused)  ;  there  is  no 
distinct  increase  of  the  percussion  dulness  ;  friction  fremitus  is 
occasionally  felt  over  the  prsecordial  region. 

3.  Cases  of  moist  pericarditis  in  zvJiicJi  the  effusion  is  not 
sufficiently  copious  to  seriously  embarrass  the  action  of  the  heart, 
and  in  ivhich  there  is  no  myocarditis  or  endocarditis. 

In  this  group,  which  includes  a  large  number  of  the  cases 
of  acute  pericarditis  met  with  in  practice,  subjective  cardiac 
sensations  due  to  derangement  of  the  heart  as  a  sensitive, 
vital  organ  (such  as  pain,  constriction  of  the  chest,  palpitation, 
etc.),  are  present,  but  mechanical  symptoms  (see  page  311) 
are  either  slight  or  altogether  absent.  The  physical  signs 
vary  with  the  stage  of  the  disease.  Pericardial  friction  is  the 
first  physical  sign  which  can  be  observed  ;  in  a  short  time, 
usually  in  a  few  hours,  dulness  on  percussion  is  developed  and 
gradually  assumes  the  characteristic  outline,  which  I  have 
previously  described  in  detail  (see  page  319);  when  the 
effusion  is  copious  the  whole  cardiac  impulse  is  raised,  the 
apex  beat  displaced  upwards  and  to  the  left,  the  force  of  the 
apex  beat  being  usually  impaired  and  sometimes  altogether 
effaced  ;  with  the  elevation  of  the  heart  the  area  of  pericardial 
friction  is  also  elevated  ;  in  young  subjects  the  precordial 
region    may  be    more    prominent    than    in    health.      As    the 


324  Diseases  of  the  Heart. 

effusion  is  absorbed,  the  area  of  cardiac  dulness  gradually 
diminishes,  the  apex  beat  regains  its  normal  position,  and  the 
friction  murmurs,  which  during  the  period  of  effusion  are, 
as  a  rule,  strictly  limited  to  the  area  of  dulness,  and  usually  to 
the  area  of  the  cardiac  impulse,  may  become  more  diffused, 
and  are  sometimes  heard  over  the  whole  of  the  sternum  and 
adjacent  parts  of  the  chest.  In  exceptional  cases  friction 
fremitus  may  now  be  felt  when  the  hand  is  placed  over  the 
praecordium. 

4.  Cases  of  moist  pericarditis  in  zvJiich  the  effusion  is  suffi- 
ciently copious  to  seriously  embarrass  the  action  of  the  heart,  and 
cases  of  pericarditis  (either  dry  or  moist)  which  are  complicated, 
with  symptoms  due  to  myocarditis  or  to  endocarditis. 

The  cases  included  under  this  group  are  attended  with 
grave  symptoms  indicative  of  serious  interference  with  the 
course  of  the  circulation,  and  with  serious  failure  of  the  action 
of  the  heart,  such  as  marked  pallor  or  livid ity  of  the  counten- 
ance, faintness,  extreme  exhaustion,  an  unusually  rapid,  weak, 
irregular,  and  dicrotic  pulse,  considerable  distention  of  the 
veins  of  the  neck,  considerable  dyspnoea  or  orthopnoea,  dropsy, 
etc.  The  physical  signs  up  to  a  certain  point  are  the  same  as 
those  described  as  characteristic  of  the  third  group,  viz.,  the 
physical  signs  proper  to  a  considerable  and  usually  progressive 
pericardial  effusion.  When  the  heart  begins  to  fail  the  friction 
murmur  usually  becomes  diminished  in  intensity  ;  and  altera- 
tions in  the  rhythm  of  the  heart  (irregular  action,  etc.)  may 
be  heard  on  listening  over  the  prsecordium.  With  the 
occurrence  of  endocarditis  valvular  murmurs  are  developed. 
It  must  not,  however,  be  supposed  that  valvular  murmurs  are 
only  heard  in  those  cases  of  pericarditis  which  are  included 
under  this  group.  In  a  large  proportion  of  the  cases  of  peri- 
carditis (of  the  rheumatic  cases  at  all  events)  which  have  been 
included  in  groups  i,  2,  and  3,  endocardial  murmurs  are 
also  present.  In  this  group  I  include  those  cases  in  which 
in  addition  to  the  valvular  murmurs,  symptoms  due  to  valvular 
lesions  are  present,  i.e.  when  the  valvular  lesion  is  sufficiently 
severe  to  mechanically  interfere  with  the  course  of  the 
circulation. 


Clinical  His  lory  of  A  title  Pericarditis.  325 

Onset,  Course,  and  Termination. 

Onset. — The  onset  is  in  many  cases  insidious,  pain  and  dis- 
comfort in  the  region  of  the  heart  being  very  generally  the 
first  symptoms  which  attract  attention.  In  other  cases,  the 
attack  is  ushered  in  by  a  feeling  of  chilliness  and  by  the  usual 
malaise,  etc.,  which  so  frequently  attend  the  commencement 
of  febrile  diseases,  very  exceptionally  there  is  a  distinct  rigor. 
In  some  cases  nausea  and  faintness  are  the  first  symptoms. 

Course. — In  acute  cases  the  inflammation  of  the  pericar- 
dium rapidly  runs  its  course, — a  fact  which  explains  the  fre- 
quent alterations  in  the  physical  signs  which  are  met  with  in  the 
disease.  In  the  course  of  three  or  four  days  the  effusion  has 
usually  reached  its  height ;  the  period  during  which  the  sac 
remains  fully  distended,  is,  as  a  rule,  brief,  in  most  cases  absorp- 
tion begins  to  occur  within  a  few  hours  after  the  effusion  has 
reached  its  highest  point.  Unless  the  case  should  become 
chronic,  which  it  only  does  in  exceptional  cases,  the  period 
during  which  the  effusion  is  stationary,  so  to  speak,  is  seldom 
longer  than  two  or  three  days.  The  period  of  absorption  and 
resolution  generally  occupies  several  days.  The  whole 
duration  of  the  attack,  from  the  commencement  to  the  dis- 
appearance of  friction,  is  usually  from  one  to  three  weeks, 
though  many  exceptions  to  this  rule  occur,  in  some  cases  the 
duration  is  shorter,  in  others  much  longer  than  that  specified. 

Termination. — The  natural  termination  of  inflammation  of 
the  pericardium,  is  recovery  with  the  formation  of  adhesions 
i.e.  with  partial  or  total  obliteration  of  the  sac.  Occasionally, 
but  very  rarely  in  cases  of  rheumatic  origin,  death  occurs 
during  the  acute  stage  ;  in  a  few  cases  the  condition  becomes 
chronic.  But  to  these  points  I  shall  again  refer  in  speaking 
of  the  prognosis. 

Diagnosis. — In  considering  the  diagnosis  of  pericarditis,  it 
is  essential  to  remember  that  the  symptoms  are  only  sugges- 
tive but  not  distinctive  ;  and  that  inflammation  of  the  pericar- 
dium can  only  with  certainty  be  recognised  by  means  of  the 
physical  signs.     Friction  sounds,  synchronous  with  the  action 


3 


26  Diseases  of  the  Heart. 


of  the  heart,  and  increased  dulness  on  percussion  of  the  form 
and  outline,  which  have  been  previously  described,  are  the 
physical  signs  of  greatest  importance  ;  but  neither  of  them  is, 
when  taken  singly,  absolutely  conclusive,  for  on  the  one  hand 
there  are  certain  conditions  in  which  sounds  are  heard  re- 
sembling those  produced  in  an  inflamed  pericardium,  and 
on  the  other,  there  are  several  conditions  in  which  dulness 
on  percussion,  resembling  more  or  less  closely  the  dulness 
due  to  pericarditis,  is  present. 

Steps  in  the  diagnosis  of  pericarditis. — When  a  case  of 
supposed  pericarditis  comes  under  observation,  we  have  there- 
fore to  determine  : — 

1.  Is  inflammation  of  the  pericardium  actually  present? 

2.  If  the  case  is  one  of  pericarditis,  what  is  the  cause  of 
the  condition,  and  what  is  the  character  of  the  effusion  ? 

3.  Is  the  case  complicated  with  myocarditis  or  endocar- 
ditis? 

Step  No.  I.  Is  the  case  one  of  pericarditis? — In  some  cases 
it  is  easy  to  decide  this  point,  in  others  difficult. 

When  a  patient,  who  has  been  previously  in  good  health, 
is  attacked  with  an  acute  illness,  more  particularly  with  one 
or  other  of  those  affections,  in  the  course  of  which  acute 
pericarditis  is  apt  to  occur  ;  and  when  a  to-and-fro  friction 
murmur  and  increased  dulness  on  percussion,  are  present 
over  the  praecordium  (more  especially  when  the  increased 
dulness  on  percussion  is  rapidly  developed  under,  as  it  were, 
the  eye  of  the  observ-er),  the  diagnosis  is  self-evident.  In 
other  cases  the  diagnosis  is  difficult ;  and  it  will  be  neces- 
sary to  consider  in  the  next  place,  the  conditions  in  which 
sounds  resembling  pericardial  friction,  or  dulness  resembling, 
more  or  less  closely,  that  produced  by  pericarditis  is  present ; 
and  the  means  by  which  they  are  to  be  distinguished. 

The  differential  diagnosis  of  pericarditis  with  friction,  and 
the  other  conditions  with  which  it  is  likely  to  be  cojifounded. 

The  typical  to-and-fro  friction  murmur  of  pericarditis  is 
of  course,  sx-nchronous  with  the  action  of  the  heart,  and  it  is 


Diagnosis  of  Acute  Pericarditis.  327 

by  this  means  at  once  distinguished  from  ordinary  pleuritic 
friction.  Cases  are,  however,  occasionally  met  with  in  which 
a  pleuritic  murmur  is  of  cardiac  rhythm.  In  \\\q  first  place, 
therefore,  we  must  consider  : — 

The  dijfereiitial  diagnosis  of  perica^-dial  friction  and  peri- 
cardial-pteurat  friction. 

In  some  cases  it  is  impossible  to  pronounce  a  positive 
opinion,  but  the  distinction  can  generally  be  made  by  atten- 
tion to  the  points  detailed  in  the  following  table  : — 

Table  I. 
TJie  Differential  Diagnosis  of  Pericardial  Friction  and 
Pericardial-pleu  rat  Friction. 
Pericardial  Friction.  Pericardial-pleural  Friction. 

Where  audible.       Usually  heard  over  the  centre     Usually  heard  over  the  borders, 
of  the  right  ventricle.  more     especially     the     left 

border,  of  the  heart. 

Effect  of  respira-    Seldom  much  affected  by  the  Always  more  or  less  affected  by 

Hon.                          respiratory  movements,  never  the   respiratory  movements; 

completely  arrested  by  hold-  often  completely  arrested  on 

ing  the  breath.     Never  act-  holding  the  breath;  often  con- 

ually*  converted  into  ordinary  verted  into  ordinary  pleural 

friction  by  a  full  inspiration  friction  by  a  full  inspiration 

or  deep  expiration.  or  deep  expiration. 

*  Note — This  point  is  not  of  much 
importance,  for  true  friction  is  not 
unfrequently  accompanied  by 
pleurisy,  and  in  cases  of  this  des- 
cription the  pericardial  friction  may 
on  a  full  respiration,  be  masked 
(though  it  is  not  actually  replaced) 
by  the  ord'nary  friction  sound. 

In  the  second  place,  pericardial  friction  is  sometimes  soft 
in  character  {i.e.  it  lacks  the  harsh  characters  which  friction 
sounds  typically  possess)  ;  and  since  a  double  murmur  is  very 
frequently  generated  at  the  aortic  orifice,  we  must  now  con- 
sider the  differential  diagnosis  of  the  double  murmur  which 
is  due  to  pericarditis  on  the  one  hand  and  to  combined  aortic 
stenosis  and  incompetence  on  the  other.  The  points  of  dis- 
tinction are  given  in  table  II. 


128 


Diseases  of  the  Heart. 


Table  II. 

Tlie  Differential  Diagnosis   of  the 

Pericarditis,    and    the    Double 

Stenosis  and  Incompetence. 

Double  Murmur  of 
Pericarditis. 


Double   Mil  mm  r  due   to 
Murmur    due    to   Aortic 


Position  ofmaxi- 
miun  intensity. 


Usually  loudest  over  the  right 
ventricle  and  lower  half  of 
the  sternum. 


Area  where  audi-    Usually  heard   over  a  limited 
ble,  and  direction     area,  and  not  propagated  over 
of  propagation.         the  course  of  the  aorta,  and 
into  the  vessels  of  the  neck. 


Relationship  to 
the  heart  sounds. 


Does  not  replace  but  only 
obscures  (more  or  less  com- 
pletely) the  heart  sounds; 
and  is  not  exactly  synchronic 
with  them. 


Double  Murmur  of  Aortic 
Stenosis  and  Incompetence. 

Although  the  diastolic  portion 
of  the  murmur  is  often  heard 
loudest  over  the  lower  end  of 
the  sternum,  it  is  also  well 
heard  at  the  base  of  the 
heart. 

Usually  heard  over  an  exten- 
sive area,  and  propagated 
over  the  course  of  the  aorta, 
and  (usually)  into  the  great 
vessels  of  the  neck. 

Does  actually  replace  (but  not 
always  completely)  the  heart 
sounds,  and  is  always  exactly 
synchronic  with  them. 


Variability. 


Effects  of  exter- 
nal pressure. 


Pulse. 


Apt  to  vary  from  day  to  day,  or 
from  hour  to  hour,  both  in 
respect  to  its  position  and 
sound  characters  ;  the  inter- 
val between  the  systolic  and 
diastolic  portions  is  not  al- 
ways of  the  same  duration, 
and  not  always  distinct. 

Almost  invariably  altered  in 
character  by  the  pressure  of 
the  stethoscope,  when  soft 
is  often  converted  into  a  rough 
friction  sound. 


Remains  constant  as  regards  its 
position  and  sound  charac- 
ters ;  the  interval  between 
the  systolic  and  diastolic  por- 
tions is  always  of  the  same 
duration  and  is  distinct. 


Uninfluenced    by  the  pressure 
of  the  stethoscope. 


Not  jerking,  visible,  collapsing     Is  jerking,  visible,  collapsing, 
or  tortuous.  and  often  tortuous. 


Condition  of  the  Not  much  altered  in  size  unless 
Icftvcntricle;  out-  previously  diseased.  Dulness, 
line  of  dulness  ;  pear-shaped  withwell-marked 
force  and  position  stalk.  Apex  beat  feeble  or 
of  apex  beat.  effaced,  tilted  upwards  and  to 

the  left. 

.Etiology.  Usually  developed  acutely   in 

the  course  of  acute  rheuma- 
tism, Bright's  disease,  etc. 


Almost  invariably  hypertro- 
phied  and  dilated — Dulness, 
heart-shaped  without  well- 
marked  stalk.  Apex  beat 
strong,  displaced  downwards 
and  to  the  left. 

May  be  developed  acutely  as 
the  result  of  rheumatic  or 
septic  endocarditis,  but  is 
usually  developed  very  gra- 
dually as  the  result  of  ather- 


Diagnosis  of  A  cute  P erica  rditis.  329 

In  the  //;/;'<:/ place  a  pericardial  friction  murmur  is  some- 
times (instead  of  being  double)  single  and  systolic  ;  and  in 
such  cases  it  may  be  mistaken  for  a  murmur  generated  within 
the  heart  itself,  i.e.  a  systolic  mitral,  tricuspid,  aortic,  or  pul- 
monary murmur.  These  are  the  cases  in  which  pericarditis 
is  liable  to  be  mistaken  for  endocarditis  ;  the  mistake  is  most 
likely  to  be  made  when  the  pericardial  murmur  is  soft  in 
character. 

In  table  III.,  p.  330,  I  have  detailed  the  points  of  distinc- 
tion between  typical  pericarditis  and  typical  endocarditis, 
while  in  table  IV.,  p.  331,  is  given  the  differential  diagnosis 
of  those  cases  of  pericarditis,  in  which  the  murmur  is  single, 
systolic,  and  soft,  and  of  the  mitral,  tricuspid,  aortic,  and  pul- 
monary murmurs  which  are  present  in  cases  of  chronic  valvular 
lesions,  anaemia,  etc. 

In  the  fourth  place,  we  must  consider  the  differential 
diagnosis  of  increased  dulness  due  to  pericarditis  and  increased 
dulness  due  to  other  conditions.  Simple  serous  effusion  into 
the  sac  of  the  pericardium  (hydropericardium)  and  enlarge- 
ment of  the  heart  itself  (more  especially  dilatation  of  the 
heart),  are  the  conditions  included  under  this  group  which 
are  most  likely  to  give  rise  to  difficulty. 

TJie  differential  diagnosis  of  increased  dulness  due  to  peri- 
carditis and  simple  dropsy  of  the  pericardial  sac. 

In  both  of  these  conditions  the  form  and  outline  of  the 
dulness  are  the  same,  but  the  diagnosis  can  usually  be  made 
without  difficulty,  by  attention  to  the  points  detailed  in  table 

v.,  p.  332. 

The  differential  diagnosis  of  pericardial  effusion  a)id  enlarge- 
ment of  the  heart  itself,  is  a  point  of  considerable  practical  im- 
portance ;  for  an  enlarged  (more  especially  a  dilated)  heart 
has  been  more  than  once  punctured  under  the  impression  that 
the  case  was  one  of  effusion  into  the  pericardial  sac.  The 
points  to  which  attention  should  be  directed  in  making  the 
distinction  are  shown  in  table  VI.,  p.  333. 


130 


Diseases  of  the  Heart. 


Table  III. 

TJic  Differential  Diagnosis  of  Acute  Pericarditis  and  A  en te 
Endocarditis. 


I.   Chai-aders  of 
the  murmur. 

{a)  Rhythm  of 
murmur. 


[b)  Sound  char- 
acters. 


(c)  Position  of 
maximum  in- 
tensity. 


{d)  Direction  of 
propagation. 


(^)  Variability. 


(/)  Effectsof pres- 
sure. 


2.  Outline  of  dul- 
ness  on  per- 
cussion. 


Pericarditis. 

In  typical  cases  a  double  (to- 
and-fro)  murmur,  which  ob- 
scures, but  does  not  actually 
replace  the  heart  sounds,  and 
which  is  not  exactly  syn- 
chronic with  them.  Excep- 
tionally the  murmur  is  single 
and  systolic. 


In  typical  cases  a  harsh  friction 
sound  ;  exceptionally,  soft ; 
superficial. 

Usually  over  the  right  ventricle, 
but  only  accidentally,  having 
its  point  of  differential  max- 
imum intensity  in  the  mitral 
and  tricuspid  areas. 

Usually  very  limited  in  area, 
and  not  propagated  in  any 
of  the  definite  lines  of  pro- 
pagation of  endocardial  mur- 
murs. 

Character  liable  to  change 
(position,  loudness,  harsh- 
ness, etc.,)  within  brief  pe- 
riods of  time. 

Almost  always  intensified,  and 
often  modified  in  other  re- 
spects, by  the  pressure  of  the 
stethoscope. 

Area  of  dulness  often  increased, 
and  pear-shaped  (see  p.  321). 


J.  Impulse,  apex-  Feeble    or   effaced  ;    if  much 
beat.  effusion  apex  tilted  upwards 

*  and  to  the  left. 


Endocarditis. 

In  the  majority  of  cases  the 
murmur  is  single  and  systolic, 
occasionally  double  (aortic). 
The  murmur  replaces  one  or 
other  of  the  heart  sounds, 
and  is  exactly  synchronic 
with  it. 
Note. — Exception  in  the  case  of  pre" 
systolic  murmurs,  which  are  how- 
ever rarely  due  to  acute  endo- 
carditis 

Usually  soft  and  blowing,  deep- 
seated. 


In  the  mitral,  tricuspid,  aortic 
or  pulmonary  areas. 


May  be  heard  over  an  extensive 
area,  and  propagated  in  cer- 
tain definite  directions  (see 
table  VIII.,  p.  527). 

Character  more  constant. 


Not  modified  by  pressure. 


Dulness  not,  as  a  rule,  much 
increased  ;  its  exact  outline 
depends  on  the  cavity  or  cavi- 
ties of  the  heart  which  are 
enlarged. 

Impulse  may  be  strong  ;  apex 
in  normal  position.  If  the 
left  ventricle  is  hypertrophied , 
apex  displaced  downwards 
and  to  the  left  ;  if  the  right 
ventricle  is  enlarged,  impulse 
may  be  in  the  pit  of  the  epi- 
gastrium. 


4.   Pain  over  the 
pracordia^  and 
tenderness  in  epi- 
gastrium. 


Usually  present. 


Usually  absent. 


Diagnosis  of  Pericarditis. 


331 


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332  Diseases  of  the  Heart. 

Table  V. 

The  Differential  Diagnosis  of  increased  Dulncss  due  to 
Pericarditis  and  Hydropericardiuni . 


Pericarditis. 

Pericardial fric-     Usually    present,    even  at   the 

iion.  height  of  the  effusion  ;  always 

present  at  some  stage  of  the 

case,  i.e.  before  or  after  the 

height  of  the  effusion. 

Subcutatuous  Usually    absent,    unless    com- 

dropsy  ajid  cffii-      plications  (great  venous  en- 

sion  into  other        gorgement     from     pressure, 

scrolls  sacs.  valvular      lesions,      Bright's 

disease,  etc.) 


Fever. 


Usually  present. 


Hydropericardiuni. 

Absent. 


Hydropericardium  is  part  and 
parcel  of  a  general  dropsy, 
and  usually  a  late  event  in 
that  condition. 


Absent,  unless  some  complica- 
tion. 


Pain  over  pra- 
cordia,  and  ten- 
derness oil  pres- 
sure in  epigas- 
trium. 

ALtiology. 


Usually  present. 


Usually  occurs  in  the  course  of 
acute  rheumatism  and  cir- 
rhotic Bright's  disease,  etc. 


Seldom  observed. 


Usually  in  the  terminal  stages 
of  mitral  lesions  ;  or,  in  the 
course  of  Bright's  disease, 
more  especially  the  acute 
form,  and  the  large  white 
chronic  variety. 


The  differe)itial  diagnosis  of  pericardial  effusion  and  of  dila- 
tation of  the  heart. — The  difficulty  chiefly  occurs,  when  the 
patient  comes  under  observation  with  the  pericardial  dulness 
already  developed,  and  more  especially  in  those  cases  in 
which  it  is  stationary  and  chronic,  and  when  there  is  no  peri- 
cardial friction.  In  both  conditions  (pericarditis  with  effusion 
and  dilatation  of  the  heart)  there  is  increased  dulness  on  per- 
cussion over  the  prsecordia,  a  feeble  impulse,  usually  feeble 
sounds,  and  often  dyspnoea,  venous  engorgement,  dropsy,  etc. 
In  order  to  arrive  at  a  correct  conclusion,  an  accurate  examin- 
ation of  the  heart,  and  careful  inquiry  into  the  previous  history 
of  the  case,  and  the  other  points  detailed  in  the  following  table 
are  indispensable 


Diagnosis  of  Pericarditis. 


Zo 


o  J 


Table  VI. 

TJie  Differential  Diagnosis  of  increased  Dtdness  dne  to 
Pericarditis  and  Dilatation  of  the  Heart. 


Pericarditis  with  Effusion. 


Dilatation  of  the  Heart. 


Outline  of  Did-  Dulness  pear-shaped,   and  en- 
ness.  largement  chiefly  upwards. 


Dulness  not  pear-shaped,  and 
enlargement  chiefly  down- 
wards. 


Rate   of  develop-  Oftenrapid,  and  then character- 
me7it    of  Dill-      istic. 

ness. 


Usually  very  slow ;  though  a 
rapid  dilatation  of  the  heart 
sometimes  occurs. 


Imptilse  and  apex-  The  impulse,  when  present,  is  Impulse  can  usually  be  felt  to 

beat.                          in  the  3d  or  4th  left  inter-  the  left  of  the  lower  end  of 

space  ;   apex  beat  tilted  up-  the  sternum,  or  in  the  epi- 

wards    and    outwards,    or  gastrium. 
effaced. 


Relation    of  did-  Dulness  may  extend  to  the  left 
ness  to  left  apex-       of  the  left  apex-beat. 
beat. 

Auscultation.  Pericardial  friction  maybe  pre- 

sent ;    when  absent,  sounds 
are  obscured. 

Pain     over  pra-  Often  present. 
cordia  atid  ten- 
derness in  epi- 
gastrium. 

Pulsation   in  the  May  be  present  if  endocarditis 
veins  of  the  neck.       complicates. 


Aetiology. 


Fever 


Usually  acute,  in  course  of 
acute  rheumatism,  cirrhotic 
Bright's  disease. 


Often  present. 


Dulness  does  not  extend  to  the 
left  of  left  apex  beat. 


Pericardial  friction  not  present  ; 
sounds  short,  but  usually 
clear. 


Usually  absent. 


Often  present  when  right  heart 
dilated. 

Usually  chronic  ;  often  associ- 
ated with  chronic  valvular 
lesions,  fatty  and  fibroid  de- 
generation, anaemia,  etc. 

Absent  unless  from  some  com- 
plication. 


The  differential  diagnosis  of  increased  dulness  due  to 
pericardial  effusion  and  hypertroph)-  of  the  heart,  can  usually 
be  made  without  difficulty.     (See  table  VII.) 


134 


Diseases  of  the  Heart. 


Table  VII. 

The  Differe7itial  Diagnosis  of  increased  D illness  due  to 
Pericarditis  and  Hypertrophy  of  the  Heart. 


Pericarditis  with  Effusion. 
Outline    of   dul-  See  remarks  in  Table  VI. 


Hypertrophy. 

See  remarks  in  Table  VI. 


Rate  of  develop-  Usually  rapid. 
ment. 


Impulse;  apex- 
beat. 


Pulse. 


Impulse,  when  present,  is  in  the 
3d  or  4th  left  interspace,  and 
is  feeble ;  apex  tilted  upwards 
and  outwards,  or  beat  effaced. 


Weak  and  quick  ;  maybe  para- 
doxical. 


Pericardial    fric-  Often  present. 
tion. 


Usually  slow. 


Impulse  powerful ;  if  left  ven- 
tricle hypertrophied,  apex 
displaced  downwards  and 
outwards  ;  if  right  ventricle 
hypertrophied,  apex  dis- 
placed downwards  and  in- 
wards, beat  may  be  in  the 
epigastrium.. 

Character  of  the  pulse  depends 
on  the  side  of  the  heart 
which  is  hypertrophied,  and 
the  cause  of  the  hypertrophy. 
When  left  ventricle  hyper- 
trophied, and  no  aortic  ob- 
struction or  mitral  regurgi- 
tation, the  pulse  is  large  and 
powerful. 

Absent. 


Prognosis. — In  considering  the  prognosis  of  pericarditis, 
we  have  to  take  into  account,  firstly,  the  danger  to  hfe 
involved  by  the  attack  itself  {i.e.  the  immediate  prognosis), 
and  secondly  (in  those  cases  which  recover),  whether  the  ad- 
hesions, which  almost  always  remain,  to  a  greater  or  less  ex- 
tent, after  a  severe  attack  of  pericarditis,  will  be  likely  to 
produce  any  permanent  or  after  bad  effect  upon  the  action 
of  the  heart.  The  remote  prognosis  is  practically,  therefore, 
synonymous  with  the  prognosis  of  '  adherent'  pericardium. 

TJie  immediate  prognosis. — The  danger  to  life  depends 
upon  the  following  conditions  :— 

(i)  The  CBtiological  cause  of  the  condition. — Uncomplicated 
cases  of  rheumatic  pericarditis  almost  always  recover.     Peri- 


Prognosis  of  Ac  life  Pericarditis.  335 

carditis  due  to  traumatic  injury,  wounds  of  the  sac,  etc.,  is 
less  serious  than  pericarditis  which  follows  the  rupture  of 
an  abscess  (in  the  liver  for  example)  into  the  sac.  Peri- 
carditis occurring  in  the  course  of  Bright's  disease  is  very 
generally  fatal ;  the  prognosis  is  still  worse  in  cases  of  purpura 
and  scurvy  ;  while  tubercular  is  almost  invariably,  and  cancer- 
ous pericarditis  always  fatal. 

(2)  The  severity  of  the  associated  diseased  condition,  and  of 
tJie  pericardial  inflammation  itself. — Other  things  being  equal, 
a  dry  is  less  serious  than  a  moist  pericarditis,  while  in  the 
latter  form,  the  more  copious  the  effusion,  the  worse  the  prog- 
nosis. In  both  varieties,  however,  tJie  condition  of  tJie  cardiac 
muscle,  and  the  state  of  the  valvular  apparatus,  are  the  two  most 
important  (cardiac)  elements  which  determine  the  prognosis, 
the  presence  of  myocarditis  being  especially  unfavourable. 

The  form  of  the  pericarditis,  whether  acute  or  chronic, 
is  also  of  importance,  chronic  pericarditis  being  very  often 
fatal.  When  the  effusion  consists  of  pus,  the  prognosis  is 
also  much  more  unfavourable  than  in  simple  cases. 

(3.)  The  presence  of  complications,  and  the  previous  state  of 
health  of  the  patient. — The  opinion  must  of  course  be  based 
upon  the  exact  nature  of  the  complication.  Hyperpyrexia, 
with  severe  cerebral  symptoms,  occurring  in  the  course  of 
rheumatic  pericarditis  is  a  very  serious  complication  ;  while 
the  fact  that  the  heart  was  diseased  before  the  attack  of 
pericarditis  commenced,  adds  considerably  to  the  danger. 
Other  things  being  equal,  a  robust,  healthy  person  will  be 
more  likely  to  survive  an  attack  of  pericarditis  than  a  weakly 
delicate  individual.  But  we  find  many  exceptions  to  this 
general  rule. 

(4.)  The  age  of  the  patioit. — In  very  young  or  very  old 
subjects,  the  prognosis  is  much  more  unfavourable  than  at 
other  periods  of  life. 

Treatment. — In  considering  the  aetiology,  I  have  pointed 
out  that  in  a  large  proportion  of  cases,  pericarditis  is  second- 
ary ;  and  that,  in  some  cases,  the  inflammation  of  the  peri- 
cardium   occurs    in   the   course  of   certain   ereneral   affections 


336  Diseases  of  the  Heart. 


(acute  rheumatism,  Bright's  disease,  etc.)  ;  in  others,  it  is  due 
to  the  direct  extension  of  pre-existing  inflammation  from 
some  neighbouring  organ  or  part  (the  pleura,  mediastinum, 
lung,  etc.) ;  while  in  a  third  group  of  cases,  it  results  from 
the  secondary  deposits  of  a  tubercular,  sarcomatous,  or  can- 
cerous nature  in  the  tissues  of  the  pericardium.  Now,  in 
treating  the  many  different  primary  affections,  which  are 
included  in  these  three  groups,  it  is  essential  to  keep  this 
tendency  to  pericarditis  prominently  in  view,  to  protect  the 
patient  most  scrupulously  from  everything  likely  to  act  as 
an  exciting  cause  or  to  arouse  the  inflammation  of  the  peri- 
cardial sac,  in  short  to  adopt,  so  far  as  we  are  able,  a  preventa- 
tive plan  of  treatment. 

It  is  no  less  important  in  managing  the  primary  affec- 
tions, to  examine  the  heart  carefully  from  time  to  time,  and 
to  look  out  for  the  first  symptoms  and  signs  of  local  mischief, 
in  order  that  we  may,  if  possible,  cut  short  and  allay  the 
pericardial  mischief  as  soon  as  it  appears  ;  while,  in  treating 
cases  of  secondary  pericarditis,  after  the  pericardial  inflamma- 
tion has  fully  developed,  one  of  the  points  to  which  attention 
must  be  prominently  directed  is  the  treatment  of  the  primary 
affection. 

Tlie  prevention  of  pericarditis. — Speaking  generally,  we 
may  say  that  the  best  method  of  preventing  secondary  peri- 
carditis is  to  remove  as  soon  as  possible  the  primary  affection, 
guarding  the  patient  at  the  same  time  from  everything  which 
is  likely  to  excite  the  inflammation  of  the  pericardium  itself. 

Some  of  the  primary  affections,  in  the  course  of  which 
pericarditis  is  apt  to  occur,  such  for  instance  as  chronic 
Bright's  disease  and  cancer,  resist  our  present  therapeutic 
means  of  cure  ;  and  in  them  we  must  content  ourselves  with 
guarding  the  patient  against  exposure  to  cold,  and  anything 
which  will  excite  or  depress  the  action  of  the  heart.  Others, 
as  for  example,  acute  rheumatism  and  some  cases  of  local 
inflammation  in  the  neighbourhood  of  the  pericardium,  can 
be  successfully  controlled  by  a  well  directed  and  energetic 
plan   of  treatment.      In   acute   rheumatism,   for  instance,  we 


Ti-catnieui  of  Acute  Pericarditis.  337 

endeavour  to  cut  short  the  attack  by  saturathig  the  system 
with  sahcin  or  saHcylate  of  soda  ;  allaying  excessive  pain, 
should  it  be  necessary,  by  hypodermic  injections  of  morphia  ; 
guarding  the  patient  from  cold  by  placing  him  in  blankets  and 
a  flannel  night  gown  to  absorb  the  excessive  perspiration,  by 
warming  the  stethoscope  and  avoiding  any  undue  exposure  of 
the  pr^Ecordium  in  making  a  routine  examination  of  the  heart  ; 
and  carefully  avoiding  everything  which  will  be  in  the  least 
likely  to  excite  or  injuriously  depress  the  action  of  the  heart.^ 
It  would  be  out  of  place  to  detail  here  the  manner  in 
which  the  different  primary  affections  are  to  be  dealt  with,  I 
therefore  pass  to  the  treatment  of  the  pericardial  inflammation 
itself 

The  treatment  of  tJie  pericardial  inflammation  itself. — In 
dealing  with  a  recently  developed  case  of  pericarditis,  it  is 
essential  to  remember,  as  Dr  Sturges  has  so  ably  pointed  out, 
and  as  I  have  for  a  long  time  been  in  the  habit  of  teaching, 
that  an  inflammation  of  the  pericardium  differs  from  many 
other  inflammations  in  this  important  particular,  viz.,  that 
although  it  seldom   is  of  itself  directly  fatal,  it  frequently  is 

'  I  am  aware  that  statistics  seem  to  show  that  salicin  and  salicylate  of  soda 
do  not  prevent  rheumatic  pericarditis  and  other  cardiac  complications.  It  will 
not,  however,  be  disputed,  that  the  rheumatic  symptoms  proper  (the  fever,  the 
joint  affection  and  the  pain)  are  speedily  relieved  by  these  drugs  ;  and  I  find 
it  difficult  to  believe  that  any  plan  of  treatment,  which  is  able  to  cut  short  the 
rheumatic  fever  itself,  will  not  in  many  cases  prevent  the  occurrence  of  pericarditis, 
provided  that  it  is  energetically  enforced  before  the  pericardial  inflammation  is 
established.  Sibson's  observations  as  to  the  influence  of  pain  and  cardiac  excite- 
ment in  the  production  of  rheumatic  pericarditis  seem  to  lend  additional  support 
to  this  view.  The  difficulty  in  arriving  at  a  conclusion  from  statistics  as  to  the 
influence  of  salicin  in  preventing  rheumatic  pericarditis  and  other  cardiac  com- 
plications is  considerable.  In  many  cases,  no  doubt,  the  signs  of  pericarditis  are 
first  detected  after  the  salicin  plan  of  treatment  has  been  commenced,  but  it  is 
unfair  to  lump  all  cases  together,  and  to  say  that  salicin  does  not  prevent 
rheumatic  pericarditis ;  in  some,  the  pericarditis  was  without  doubt  actually 
present  though  undetected  or  undetectable  before  the  treatment  was  commenced  ; 
in  others,  the  pericardial  inflammation  was  developed  before  the  system  was 
properly  saturated  with  the  drug.  It  is  only  the  remainder,  viz.,  those  in  which 
the  pericardial  inflammation  developed  after  full  saturation  of  the  system  that  can 
be  legitimately  adduced  in  evidence  ;  and  we  want,  I  think,  more  information  on 
this  point.     (This  subject  is  afterwards  considered  in  greater  detail,  see  p.  3^^-) 


338  Diseases  of  iJie  Heart. 

followed  by  secondary  changes,  which  cripple  the  vitality  of  the 
patient,  and  which  lead  to  the  subsequent  disease,  and  it  may  be 
to  an  early  death.  A  lung,  for  example,  which  has  been  affected 
with  croupous  pneumonia,  however  severe,  is  (in  the  great 
majority  of  instances)  to  all  intents  and  purposes  as  sound  as 
it  was  before  ;  but  a  heart  after  a  severe  attack  of  pericarditis 
is,  in  many  cases,  permanently  damaged,  in  consequence,  not 
only  of  the  adhesions  which  remain,  but  also — and  this  is 
much  more  important — because  of  the  strong  tendency  which 
the  inflammatory  process  has  to  make  its  way  to  the  deeper 
structures,  and  to  leave  permanent  structural  alterations  in 
the  muscular  walls  of  the  organ. 

As  soon,  then,  as  there  is  any  evidence  of  local  mischief, 
it  is  all  important  to  do  what  we  can  to  cut  short  and  allay 
the  inflammatory  process  in  the  pericardial  sac. 

The  patient  should,  if  possible,  be  placed  in  a  well  venti- 
lated and  airy  room,  the  temperature  of  which  must  be  con- 
tinuously kept  between  65°  and  70°  Fahr.  Absolute  rest  in 
the  recumbent  position  must  be  rigidly  enforced,  and  every- 
thing which  tends  to  excite  the  action  of  the  heart  avoided. 
A  full  dose  of  quinine,  in  combination  with  morphia,  as 
recommended  by  Professor  Robert  Bartholow,^  should  be 
administered  ;  and  local  means  employed  to  restrain  those  vas- 
cular changes  which  accompany  eveiy  inflammation. 

In  robust  and  previously  healthy  individuals,  and  more 
especially  in  those  in  whom  the  pnlse  is  strong  and  tense,  the 
local  abstraction  of  blood  should  be  practised,  six,  eight,  or 
ten  leeches  being  applied  over  the  proecordial  region.  The 
continuous  application  of  cold  to  the  region  of  the  heart  by 
means  of  ice-bags  is  next  recommended,  more  especially  by 
German  writers.  Personally,  I  have  no  experience  of  this  plan 
of  treatment,  for,  in  common  with  most  English  physicians,  I 
have  been  in  the  habit  of  recommending  warm  applications  or 
a  mustard  poultice,  followed  by  the  continuous  application  of 

'  Bartholow  recommends  the  administration  of  a  full  dose  of  quinine  (15-20 
grains  of  the  sulphate)  with  a  quarter  to  half  a  grain  of  morphia,  '  and  the  cin- 
chonism  should,'  he  saj's,  '  be  maintained  by  repeated  smaller  doses,  for  twenty- 
four  hours  or  longer.' — Practice  of  Medichu,  second  edition,  p.  237. 


I 


Treatment  of  Acute  Pericarditis.  339 

heat,  by  means  of  hot  poultices  or  fomentations,  to  the  prai- 
cordia,  I  can  easily  conceive,  however,  that  in  suitable  cases 
(in  robust  and  previously  healthy  individuals,  and  quite  at  the 
commencement  of  the  attack)  the  continued  application  of 
cold  may  be  beneficial.  Excessive  and  violent  action  of  the 
heart  should  be  restrained  by  the  frequent  administration  of 
small  doses  of  aconite^  or  veratrum  viride. 

The  administration  of  aconite  is  recommended  by  Pro- 
fessor Sydney  Ringer  '  in  pericarditis  accompanied  with 
violent  throbbings  and  extreme  pain.'"' 

Pain  in  the  region  of  the  heart  should  be  relieved  by 
subcutaneous  injections  of  morphia  ;  and  even  in  those  cases 
in  which  there  is  little  or  no  pain,  the  administration  of  small 
doses  of  opium  or  morphia  is  often  very  beneficial. 

I  must  repeat,  that  depletion,  continuous  cold,  aconite  and 
veratrum  viride  are  only  permissible  in  robust  and  previously 
healthy  individuals,  especially  in  those  in  whom  the  pulse 
is  strong  and  tense  ;  and  also,  that  it  is  important  in  all  cases 
in  which  these  remedies  are  employed,  to  keep  a  watchful 
eye  upon  the  condition  of  the  heart  and  pulse,  for  it  is 
essential  to  avoid  anything  which  depresses  the  action  of  the 
heart.  Leeches,  continuous  cold,  aconite  and  veratrum,  are 
useful  so  long  as  they  are  employed  merely  to  moderate  exces- 
sive action,  they  are  injurious  when  they  are  pushed  beyond 
this  point,  and  allowed  to  produce  depression. 

The  treatment  appropriate  to  the  primary  affection  must, 
at  the  same  time  be  persevered  with.  There  is,  however, 
one  very  important  exception  to  this  general  rule,  viz.,  that 
in  rheumatic  cases  the  further  administration  of  the  pre- 
parations of  salicin  (more  especially  salicylate  of  soda,  for, 
according  to  Dr  Maclagan,  salicin  itself  does  not  depress  the 
heart)  should  be  dispensed  with.  The  diet  should  be  light 
and  nutritious,  consisting  chiefly  of  milk  and  soups. 

As  soon  as  the  excessive  action  of  the  heart  has  been 
moderated,  or,  if  at  the  end  of  twenty-four  or  thirty-six  hours 

'   In  cases  of  albuminuric   pericarditis  (pericarditis  occurring  in   the  course  of 
rright's  disease)  opium  if  given  at  all,  must  be  administered  cautiously. 
^  Handbook  of  Therapeutics,  ninth  edition,  p.  472. 


340  Diseases  of  tJic  Heart, 

the  inflammatory  process  is  not  arrested,  the  aconite  or  vera- 
trum  should  be  discontinued  ;  and  it  is,  in  many  cases,  advis- 
able to  discontinue  the  ice-bags,  and  to  apply  poultices,  fomen- 
tations, or  soothing  liniments,  containing  opium,  chloroform, 
belladonna,  etc.,  to  the  pr.xcordium.^ 

The  subsequent  treatment  of  the  case  must  be  modified 
in  accordance  with  the  form  of  the  disease  (whether  dry  or 
moist),  the  severity  of  the  attack,  the  general  constitutional 
state,  etc. 

It  is  difficult  to  lay  down  general  rules  applicable  to  all 
cases.  The  following,  however,  may  be  said  to  be  the  chief 
indications  for  treatment. 

1.  To  allay  the  inflammatory  process. — The  same  general 
measures  should  be  continued  as  were  recommended  in  the 
earliest  stages  of  the  attack  (absolute  rest,  the  avoidance  of 
anything  likely  to  excite  the  action  of  heart,  a  light  diet, 
etc.).  When  the  fever  is  considerable,  the  quinine  may  be 
continued,  with  or  without  a  diaphoretic.  Warm  poultices  or 
anodyne  fomentations  are  to  be  continually  applied  to  the 
praecordial  region. 

2.  To  relieve  symptoms. — Pain  is  to  be  relieved  by  local 
anodyne  applications,  or  the  internal  or  subcutaneous  ad- 
ministration of  opium  or  morphia.  Sleeplessness,  which  is 
often  a  distressing  symptom,  is  also  best  relieved  by  an 
opiate  at  bedtime.  Where  there  is  no  pain,  chloral,  or  chloral 
combined  with  bromide  of  potassium,  may  be  substituted  ; 
personally  I  prefer  opium  or  morphia,  for  chloral  is  apt  to 
have   a    depressing    influence    upon    the    heart.     Xausea  and 

'  Modifications  in  the  vascularity  of  the  pericardium  may  probably  be  produced 
in  two  ways  by  means  of  external  application,  viz. : — 

(i.)  Directly,  through  the  communications  which  exist  between  the  subcutane- 
ous vessels  of  the  chest  wall  and  the  vessels  on  the  outside  of  the  pericardial  sac. 
By  depleting  the  subcutaneous  vessels  by  means  of  leeches,  we  deplete  at  the  same 
time  the  vessels  on  the  outside  of  the  pericardial  sac  ;  and  by  producing  dilatation 
of  the  subcutaneous  vessels  by  the  application  of  a  warm  poultice,  we  draw  blood 
from  the  vessels  in  the  exterior  of  the  pericardium  which  communicate  with  them. 

(2.)  Indirectly,  by  reflex  nervous  impulses.  This  is  probably  the  more  im- 
portant of  the  two,  for  by  this  means  we  can  probably  act  not  only  upon  the  exterior 
of  the  visceral  pericardium,  but  also  upon  the  interior  of  the  parietal  pericardium, 
and  indeed  upon  the  vascularity  of  the  heart  itself. 


Trcatniciit  of  Acute  Pericarditis.  341 

sickness,  which  arc  not  unfrequent,  and  are  often  distressing 
symptoms,  are  best  reheved  by  sucking  ice,  the  appHcation 
of  a  mustard  bhster  to  the  pit  of  the  epigastrium,  and  the 
internal  administration  of  champagne,  brandy,  morphia,  or 
hydrocyanic  acid.  Dyspncca  is  often  met  with  in  the  later 
stages  of  the  attack  ;  it  may  depend,  as  we  have  previously 
seen,  upon  many  different  conditions,  amongst  which  failure 
of  the  action  of  the  heart,  valvular  complications,  the  pressure 
of  a  large  pericardial  effusion  upon  the  trachea  or  left  bron- 
chus, and  lung  complications  (such  as  pleurisy  and  pneumonia) 
are  the  chief.  Each  of  these  forms  of  dyspnoea  will,  of  course, 
require  a  special  plan  of  treatment.  When,  for  instance,  the 
shortness  of  breath  is  due  to  failure  of  the  heart's  action, 
cardiac  tonics  and  stimulants  should  be  freely  administered  ; 
when  the  dyspnoea  is  urgent,  and  when  it  depends  upon  the 
mechanical  pressure  of  a  large  effusion,  aspiration  of  the  peri- 
cardium should  be  practised. 

Hyperpyrexia  is,  as  we  have  previously  seen,  occasionally 
developed  in  the  course  of  rheumatic  pericarditis.  Prompt 
measures  should  be  at  once  taken  to  reduce  the  temperature, 
and  amongst  these  the  cold-bath  treatment  appears  to  be 
by  far  the  best.  The  patient  should  be  immersed  in  a  bath 
at  95°-ioo°  Fahr.,  cold  water  should  gradually  be  added  until 
in  the  course  of  twenty  minutes  or  half  an  hour  the  tem- 
perature of  the  bath  is  reduced  to  60°  Fahr.  If  there  is 
any  tendency  to  cardiac  depression,  it  is  a  good  plan  to 
give  a  small  quantity  of  brandy  both  before  and  after  the 
bath.  The  patient  should  at  once  be  removed  from  the  bath 
if  any  serious  symptoms  of  cardiac  depression  arise.  In 
private  practice,  or  when  it  is  inconvenient  to  immerse  the 
patient  in  a  bath,  the  application  of  iced-cloths,  in  the 
manner  recommended  by  Professor  Sydney  Ringer,^  may  be 
substituted. 

3.  To  sustain  the  strength  of  the  patient,  and  in  particular 
should  any  indications  of  cardiac  failure  arise,  to  stimulate  and 
strengthen  the  action  of  the  heart. 

This  is  a  most  important  indication,  for  one  of  the  great 

'  Handbook  of  ThcrapcuiUs,  ninth  edition,  p.  6i. 


342  Diseases  of  the  Heart. 

dangers  in  pericarditis  is  failure  of  the  action  of  the  heart.  A 
watchful  eye  should  always  be  kept  upon  the  pulse  and 
venous  circulation.  When  the  heart's  action  is  irritable  and 
weak,  digitalis  or  convallaria  majalis  should  at  once  be 
administered,  the  dose  depending,  of  course,  upon  the  special 
circumstances  of  each  case.  Alcoholic  stimulants  (brandy), 
carbonate  of  ammonia,  or  spirits  of  chloroform,  should  be 
given  in  those  cases  in  which  there  is  rapid  failure  of  the 
heart. 

4.  To  promote  absorption  of  the  inflammatory  products. — In 
the  majority  of  cases,  the  inflammatory  products  are  more  or 
less  rapidly  absorbed  soon  after  the  acme  of  the  effusion  has 
been  reached  ;  but  this  is  not  always  the  case,  and  it  is  often 
desirable  to  assist  the  natural  process  of  absorption.  With 
this  object,  iodide  of  potassium,  diuretics  (especially  digitalis, 
and  convallaria  majalis),  and  if  the  patient's  strength  per- 
mits, diaphoretics  are  administered  internally ;  counter  irri- 
tants (tincture  of  iodine,  small  and  frequently  repeated  fly- 
blisters,  etc.)  are  applied  over  the  praecordia  ;  while  the 
greatest  attention  is  paid  to  the  condition  of  the  general 
health,  the  treatment  in  fact  should,  so  far  as  possible, 
be  of  a  tonic  character,  the  object  being  to  raise  the  gen- 
eral tone  of  the  system,  and  in  particular  to  sustain  and 
strengthen  the  action  of  the  heart.  Digitalis  and  convallaria 
majalis,  which  are  both  powerful  cardiac  tonics  and  active 
diuretics,  are  particularly  useful.  The  diet  should  be  light, 
and  at  the  same  time  as  nutritious  as  possible ;  the  bowels 
must  be  regulated  ;  and  the  ventilation  of  the  patient's  room 
carefully  attended  to.  It  is  particularly  important  to  avoid 
all  causes  of  mental  depression,  and  in  short  to  keep  the 
patient  as  cheerful  and  hopeful  as  possible. 

5 .  When  the  effusion  is  progressing  so  rapidly  or  is  so  exten- 
sive as  to  seriously  embarrass  the  action  of  the  heart  and  endaiiger 
life,  or  when  it  refuses  to  be  absorbed  by  ordinary  treatment,  to 
zvithdraiu  the  fluid  by  aspirating  the  pericardial  sac. 

It  is  unnecessary  again  to  detail  the  symptoms,  which 
result  from  the  pressure  of  a  large  pericardial  effusion  upon 
the  heart  itself  and   upon  the  surrounding  structures,  or  the 


Treatment  of  Acute  Pericarditis.  343 

manner  in  which  a  pericardial  effusion  is  to  be  distinguished 
from  the  other  conditions  with  which  it  is  Hkely  to  be  con- 
founded, for  these  points  have  already  been  considered  (see 
pages  329,  ctseq.).  I  therefore  pass  on  to  say  that  the  operation 
has  now  been  performed  in  a  large  number  of  cases  with  com- 
plete success  ;  the  result  has  been  most  favourable  in  rheumatic 
cases  associated  with  rapid  effusion  into  the  sac  ;  it  is  much 
less  favourable  in  non-rheumatic  forms,  and  especially  when 
the  condition  has  become  chronic.  Dr  John  B.  Roberts  of 
Philadelphia,  who  has  directed  special  attention  to  the  subject, 
states  that  of  thirty-five  cases  in  which  the  operation  has  been 
performed  since  the  year  i860,  ten  recovered  and  twenty-five 
died,  giving  a  mortality  of  71-42  per  cent.  'In  the  twenty- 
five  instances  where  death  occurred  subsequent  to  the  tapping 
serious  disease  is  stated  to  have  existed  in  all  the  cases  except 
three.  In  other  words,  out  of  the  whole  thirty-five  cases 
operated  upon,  there  were  thirteen  cases  of  pericardial  effusion 
where  other  diseases  did  not  seem  to  act  as  a  complication, 
and  of  these  ten  recovered  and  three  died.  This  would  give 
a  mortality  of  23  per  cent.' 

Dr  Roberts  not  only  recommends  that  the  operation 
should  be  performed  'whenever  the  effusion  whether  it  be 
serum,  pus,  or  blood  accumulates  so  rapidly  or  in  such  quan- 
tity that  it  threatens  to  destroy  life,  and  refuses  to  undergo 
absorption  by  ordinary  treatment ; '  but  he  even  advocates 
its  use  as  a  palliative  method  of  relief,  in  cases  in  which  the 
pericardial  inflammation  depends  upon,  or  is  associated  with 
incurable  organic  conditions. 

The  sac  should  be  punctured  with  the  aspirator,  and 
with  the  strictest  antiseptic  precautions.  In  selecting  the 
point  of  puncture  we  must  avoid  the  heart  itself,  the  dia- 
phragm, the  internal  mammary  artery,  and,  if  possible  (though 
this  is  a  point  of  much  less  importance)  the  left  pleura. 
In  most  cases  the  needle  should  be  inserted  in  the  fifth 
left  interspace,  midway  between  the  nipple  line  and  the 
sternum,  just  above   the  junction  of  the    sixth    rib  with    its 

'  These  statistics,   which  are  detailed  in  Dr  Robert's  work  on  Paracentesis  of 
the  Pericardium,  page  97,  were  brought  up  to  the  year  1880. 


344  /^/scascs  of  the  Heart. 

costal  cartilage.  When  the  heart  is  enlarged  or  tied  down 
by  adhesions,  the  puncture  should  be  made  in  the  sixth  inter- 
space, or,  as  Sibson  suggests,  between  the  ensiform  cartilage  and 
the  seventh  costal  cartilage.  The  following  are  the  directions 
which  it  is  advisable  to  follow  in  performing  the  operation  : — 

(i.)  Place  the  patient  in  the  recumbent  position,  so  as  to 
allow  the  heart  to  fall  away  from  the  front  wall  of  the 
chest. 

(2.)  See  that  the  apparatus  is  in  working  order  and  per- 
fectly clean.  It  is  a  good  plan  to  draw  a  stream  of  carbolic 
solution  through  it  before  attempting  to  insert  it  into  the  sac. 

(3.)  Count  the  interspaces  accurately  from  above,  down- 
wards. 

(4.)  Percuss  and  auscultate  over  the  seat  of  the  proposed 
puncture,  and  satisfy  yourself  that  it  is  dull  on  percussion,  and 
that  the  dulness  does  not  depend  upon  the  presence  of  the 
heart. 

(5.)  Introduce  the  needle  of  the  aspirator  with  a  firm 
plunge  ;  if  the  skin  is  thick,  or  if  you  are  using  a  large  needle, 
a  preliminary  incision  through  the  skin  with  a  sharp  bistuory 
is  advisable.  The  needle  should  be  directed  at  first  directly 
backwards,  and  then  backwards  and  downwards  in  order  to 
avoid  wounding  the  heart. 

(6.)  If  after  exhausting  the  apparatus  no  fluid  passes, 
withdraw  the  needle,  wash  it  out,  and  if  you  feel  sure  of  your 
diagnosis  reintroduce  it. 

(7.)  It  is  advisable,  unless  there  is  any  indication  to  the 
contrary,  to  draw  off  all  or  a  large  portion  of  the  fluid  at 
one  sitting. 

(8.)  After  the  needle  is  withdrawn  a  piece  of  lint  should 
be  fixed  by  adhesive  plaster  over  the  superficial  wound. 

(9.)  If  pure  blood  flows  through  the  instrument,  if  the 
heart  has  been  wounded,  or  if  any  untoward  symptoms,  such 
as  acute  pain,  dyspnoea,  etc.,  should  arise  during  the  process  of 
aspiration,  the  needle  should  at  once  be  withdrawn. 

6.  WJioi  tJic  effusion  eonsists  of  pus  to  lay  open  tlie  sae, 
nneier  strict  antiseptic  preeautioiis,  and  to  insert  a  drainage  tube. 


AdJierent  Pcricardiuiu.  345 

When  the  effusion  consists  of  pus  the  case  should,  in  short,  be 
treated  as  any  other  internal  abscess.  Both  physicians  and 
surgeons  are  becoming  every  day  more  and  more  convinced 
that  whenever  there  is  an  internal  collection  of  pus  it  should 
if  possible  be  evacuated  ;  and  a  collection  of  pus  within  the 
sac  of  the  pericardium  forms  no  exception  to  the  general  rule. 
As  yet  the  operation  has  only  been  twice  performed  success- 
fully. The  details  of  the  last  case,  that  of  Dr  West,  will  be 
found  in  the  Lancet  for  April  28,  1883,  p.  728,  to  which  the 
reader  is  referred  for  further  information  on  the  subject. 

ADHERENT   PERICARDIUM. 

The  recovery  from  an  attack  of  acute  pericarditis  is  seldom 
complete,  for  in  most  cases  some  adhesions  between  the 
visceral  and  parietal  layers  of  the  sac  remain.  Sometimes 
the  whole  sac  of  the  pericardium  is  obliterated,  more  fre- 
quently the  adhesions  are  partial. 

The  adhesions  are  permanent,^  and  since  they  are  in 
some  cases  followed  by  secondary  changes  in  the  heart 
and  circulation,  and  therefore  by  permanent  bad  effects 
upon  the  health  of  the  patient,  I  must  now  describe  the 
nature  of  the  secondary  changes,  the  symptoms  and  physical 
signs  to  which  they  give  rise,  and  the  manner  in  which  peri- 
cardial adhesions  are  to  be  recognised  during  life. 

The  effects  ivhicJi  pericardial  adJicsions  produce  upon  the 
heart,  and  the  symptoms  to  which  they  give  rise,  depend  more 
particularly  upon  the  following  conditions  : — 

1.  The  extent  and  character  (more  especially  the  density) 
of  the  adhesions. 

2.  The  condition  of  the  muscular  walls  of  the  heart  after 
the  attack  of  pericarditis  has  subsided. 

3.  The  condition  of  the  valvular  apparatus  of  the  heart. 
When    the    adhesions    are    limited    in    extent,    when    the 

myocardium  and  valvular  apparatus  remain  healthy,  the 
adhesions  produce  little  or  no  effect  upon  the  condition  of 
the  heart,  and  are  unattended  with  symptoms. 

'   It  occasionally  happens  that  the  adhesions  are  afterwards   broken  down    by 
the  movements  of  the  heart. 


346  Diseases  of  the  Heart. 

When,  on  the  contrary,  the  adhesions  are  universal  and 
dense,  when  the  pericarditis  is  compHcated  with  myocarditis, 
and  an  increase  of  the  intermuscular  fibrous  tissue  remains 
after  the  attack  has  subsided,  the  muscular  walls  of  the  heart 
usually  undergo  degeneration,  the  muscular  fibres  becoming 
atrophied^  in  consequence  of  the  pressure  which  the  fibrous 
tissue  (both  on  the  surface  and  in  the  substance  of  the  organ) 
exerts  upon  them  during  its  cicatrisation.-  In  these  cases  very 
grave  symptoms,  indicative  of  failure  of  the  heart  muscle, 
which  I  shall  describe  in  detail  when  I  come  to  speak  of  the 
effects  of  myocarditis  (see  p.  564),  are  observed.^ 

In  other  cases,  again,  the  heart  becomes  hypertrophied  ; 
indeed  it  used  to  be  supposed  that  an  adherent  pericardium, 
by  embarrassing  the  action  of  the  organ,  necessitated  in- 
creased force  of  contraction,  and  consequently  produced 
hypertrophy.  We  now  know  that  although  this  is  the  se- 
quence of  events  in  some  cases,  partial  atrophy  of  the  muscu- 
lar fibres  and  dilatation  rather  than  hypertrophy  are  usually 
observed.  In  many  cases  a  combined  condition  of  partial 
atrophy  with  dilatation,  and  of  partial  hypertrophy  results  ; 
and  in  a  certain  number  of  cases  more  or  less  general  hyper- 
trophy is  found.  This  result  (hypertrophy)  is  usually  due 
to  associated  valvular  lesions,  though  it  may  be  the  direct 
result  of  the  pericardial  adhesions  independently  of  any  valvu- 
lar lesion  ;  it  is  most  likely  to  occur  in  those  cases  in  which 
the  pericardial  sac  is  adherent  to  the  front  wall  of  the  chest 
as  well  as  to  the  surface  of  the  heart,  and  in  which  the  myo- 
cardium is  healthy.^ 

In  cases  of  this  description  {i.e.  adherent  pericardium  with 

'  In  many  of  these  cases  the  weight  of  the  heart  and  the  thickness  of  its  walls 
are  not  diminished,  in  fact  they  may  be  increased.  The  atrophy  of  the  muscular 
fibres  can,  in  such  cases  only  be  detected  by  microscopical  examination. 

-  The  fibrous  tissue  which  remains  after  a  pericarditis,  contracts  just  as  the 
fibrous  tissue  in  a  cicatrix  does. 

^  It  must  be  remembered  that  increased  thickness  of  the  cardiac  walls,  and 
increased  weight  of  the  organ,  do  not  necessarily  indicate  true  hypertrophy,  i.e. 
an  actual  increase  of  the  muscular  tissue.  The  increased  weight  may  be  due  to 
an  increase  of  fibrous  tissue  and  fat,  and  may  actually  be  associated  with  atrophy 
of  the  true  muscular  elements,  as  I  have  observed  above. 


Physical  signs  of  Adhei'ent  Pe^'icardiuni.       347 

hypertrophy)  the  symptoms  are  usually  those  of  the  valvular 
lesion  which  is  so  often  present,  and  on  which,  to  a  consider- 
able extent  at  least,  the  hypertrophy  depends. 

The  physical  signs  of  adherent  pericardium. — In  some  cases, 
more  especially  when  the  adhesions  are  partial  and  confined 
to  the  interior  of  the  sac,  the  condition  is  not  attended  with 
any  distinct  physical  signs,  and  cannot^  therefore,  be  recog- 
nised during  life ;  in  other  cases,  there  are  very  distinct 
physical  signs  which  clearly  indicate  the  nature  of  the  con- 
dition ;  while  in  a  third  group  of  cases,  the  physical  signs 
are  equivocal  or  indistinct. 

The  physical  signs  characteristic  of  adherent  pericardium 
are  best  marked  in  those  cases  in  which — 

(i)  The  adhesions  within  the  sac  are  extensive  or 
universal. 

(2)  The  exterior  of  the  sac  is  adherent  to  the  chest  wall 
and  to  the  anterior  margins  of  the  lungs. 

(3)  The  heart  is  acting  powerfully,  i.e.  is  hypertrophied. 
The  condition  of  the  anterior  margin  of  the  lungs,  more 

especially  of  the  left  lung,  is  also  an  important  point.  When 
the  anterior  margins  of  the  lungs  are  tied  down  by  adhesions, 
the  physical  signs  are  more  distinct.  When,  on  the  contrary, 
the  lungs  have  free  play,  and  still  more  when  they  are  vo- 
luminous or  emphysematous,  the  physical  signs  of  adherent 
pericardium  are  obscure  and  indistinct. 

When  there  are  extensive  adhesions  both  on  the  interior 
and  exterior  of  the  pericardial  sac,  the  heart  is,  as  it  were, 
rigidly  fixed  in  the  cavity  of  the  chest,  and  the  free  play  of 
its  natural  movements  is  interfered  with.  In  consequence  of 
this  alteration  in  its  physical  condition,  the  following  altera- 
tions in  the  physical  signs  are  observed  : — 

( I )  Systolic  depression,  instead  of  systolic  protrusion  of  the 
apex  beat ;  and  in  many  cases  a  systolic  depressioji  of  the  lozver 
end  of  the  sternum  and  adjacent  costal  cartilages. — In  conse- 
quence of  the  adhesions,  the  ventricles,  during  their  contrac- 
tion, pull  directly  upon  the  diaphragm  and  front  wall  of  the 
chest,  and    it   is   to  this  traction,  aided,  of  course,   by  the 


34S  D/scascs  of  t lie  Heart. 

external  pressure  of  the  atmosphere,  that  the  systoHc  depres- 
sion of  the  apex  beat  and  front  wall  of  the  chest  is  due.  This 
systolic  depression  is  most  marked  when  the  chest  wall  is 
yielding  {i.e.  in  young  subjects),  and  when  the  ventricles  are 
acting  powerfully  {i.e.  when  the  heart  is  hypertrophied) ;  vice 
versa  it  is  absent  or  indistinct  when  the  cartilages  are  ossified, 
and  when  the  heart  is  acting  feebly  {i.e.  the  muscular  walls  of 
the  heart  degenerated,  its  cavities  dilated,  etc.) 

Systolic  depression,  instead  of  depression  of  the  apex  beat,  is  not 
absolutely  distinctive  of  pericardial  adhesions,  as  Friedreich  has  shown ; 
and  Bauer  says — '  We  may  state  in  general  terms  that  systolic  pitting  at 
the  site  of  the  apex  beat  may  be  present  in  all  cases  in  which  the  normal 
movement  of  the  heart  downwards  and  to  the  left,  with  elevation  of  the 
apex,  is  hindered,  provided  at  the  same  time  the  lungs  do  not  sufficiently 
approach  each  other,  and  the  contraction  of  the  heart  is  powerful  enough 
to  force  the  apex  away  from  the  chest  wall.  Under  such  circumstances 
the  pitting  follows,  as  a  matter  of  course,  from  atmospheric  pressure." 

(2)  Permanent  depression  of  the  precordial  region. — This 
condition,  in  which,  as  it  were,  the  temporary  systolic  depres- 
sion has  become  fixed  and  permanent,  is  only  observed  in 
those  cases  in  which  the  chest  wall  is  elastic,  and  in  which  the 
pericardium  is  extensively  adherent  to  the  heart  on  the  one 
side  and  to  the  chest  wall  on  the  other. 

(3)  A  diastolic  rebound  of  the  chest  zvall. — This  is  a  most 
distinctive  sign  of  adherent  pericardium,  and  it  is  due  to  the 
fact  that  after  the  depression  of  the  lower  end  of  the  sternum 
and  adjacent  costal  cartilages  has  taken  place,  and  when  the 
ventricle  begins  to  relax,  the  natural  elasticity  of  the  chest 
wall  causes  a  rebound,  which  can  be  distinctly  felt  by  the 
hand  as  an  impulse  during  the  diastole  of  the  heart. 

(4)  Absence  of  the  apex  beat.— In  some  cases  of  adherent 
pericardium  the  apex  beat  is  absent.  This  condition  is 
most  likely  to  occur  when  the  heart  is  acting  feebly,  or 
when  the  lungs  are  adherent  over  the  position  of  the  apex 
beat. 

In  some  cases  in  which  systolic  depression  of  the  apex 
beat  is  observed,  it  is  impossible  to  feel  the  pulsation  of  the 

'  Ziemssen'.s  Cyclop<cdia  11/ Medicine',  vol.  vi.  p.  643. 


P/iysical  si'ojis  of  ^Idhcrent  Pcricardiiiiii.        349 

apex  impulse  ;  in  other  cases  a  diastolic  impulse,  similar  in 
character  to  the  diastolic  rebound  of  the  chest  wall,  has  been 
noted. 

(5)  Fixation  of  the  apex  beat. — In  conditions  of  health 
certain  alterations  in  the  position  of  the  patient  are  attended 
with  corresponding  alterations  in  the  position  of  the  apex 
beat.  Sibson,  for  example,  has  shown  that  when  the  patient 
lies  on  his  left  side, the  apex  beat  may  be  displaced  'from  the 
fifth  interspace,  a  little  lower  than  the  nipple,  and  within  the 
mammary  line,  to  the  sixth  or  seventh  space,  two  inches  to 
the  left  of  the  line.'  Now,  in  the  conditions  which  we  are 
considering,  this — the  natural  mobility  of  the  apex  beat — 
cannot,  of  course,  take  place ;  and  whatever  the  position 
of  the  patient  the  apex  beat  remains  much  in  the  same  posi- 
tion. 

(6)  When  the  lungs  are  at  the  same  time  retracted  and 
fixed  by  adhesions,  the  area  of  perieardial  dnlness  is  not  only 
enlarged,  but  remains  of  the  same  si::e  both  during  inspiration 
and  expiration. 

This  is  not,  of  course,  distinctive  of  pericarditis,  for  it  only 
shows  that  the  anterior  margins  of  the  lungs  are  tied 'down  as 
the  result  of  pleurisy  ;  but  when  taken  in  conjunction  with 
the  other  physical  signs,  mentioned  above,  it  is  corroborative 
of  the  presence  of  an  adherent  pericardium. 

(7)  Distention  of  the  veins  of  the  neck  during  the  systolic 
depression  of  the  chest  zvall  (i.e.  during  the  systole  of  the  ven- 
tricles^, folloiued  by  their  rapid  collapse  and  disappearance 
during  the  diastolic  rebound  (i.e.  during  the  diastole  of  the 
heart)  is  another  important  sign,  which  was  first  described  by 
Friedreich.  It  is  due  to  the  fact,  that  during  the  systolic 
depression  of  the  chest  wall,  the  cavity  of  the  chest  is 
diminished  in  size,  and  a  mechanical  hindrance  offered  to  the 
return  current  of  blood  through  the  superior  cava.  During 
the  diastolic  rebound,  on  the  other  hand,  the  cavity  of  the 
chest  is  suddenly  expanded,  a  suction  force  is  exerted,  and 
the  previously  distended  veins  are  in  consequence  suddenly 
emptied. 


35©  Diseases  of  the  Heart. 

Indurative-mediastino-pcrkarditis.  When  in  addition  to 
the  adhesions  which  rigidly  fix  the  heart,  as  it  were,  in  the 
cavity  of  the  thorax,  the  cellular  tissue  of  the  mediastinum  is 
implicated  by  the  inflammation,  and  fibrous  adhesions  are 
formed  between  the  chest  wall  and  the  lungs  on  the  one  hand, 
and  the  great  vessels  at  the  base  of  the  hearL^  (the  aorta  and 
its  branches  and  the  superior  vena  cava)  on  the  other,  the 
passage  of  the  blood  from  the  heart  through  the  aorta  and  its 
branches,  and  to  the  heart  through  the  superior  cava,  may  be 
interfered  with. 

This  interference  with  the  circulation,  through  the  aorta 
and  vena  cava,  only  occurs  when  the  adhesions  are  put  upon 
the  stretch  ;  and  it  is  due  to  the  fact  that  the  tense  adhesions 
constrict  the  blood  vessels,  and  thereby  produce  a  mechanical 
hindrance  to  the  circulation.  And  since  the  adhesions  are 
put  upon  the  stretch  by  the  expansion  of  chest  wall  and  lungs 
which  occurs  during  the  effort  of  inspiration,  it  follows  that 
the  interference  with  the  circulation  through  the  aorta  and  its 
branches,  and  through  the  vena  cava  superior  is  only  observed 
during  the  same  period,  i.e.  during  inspiration. 

The  obstruction  to  the  passage  of  the  blood  through  the 
aorta  produces  a  peculiar  alteration  in  the  character  of  the 
pulse,  to  which  the  terras  pulsus  paradoxus  ^.nd  pulsus  inspira- 
tione  intevjuitteus  have  been  given.  As  the  latter  term  indi- 
cates, the  alteration  consists  in  the  fact  that  the  pulse  becomes 
much  diminished  in  volume,  or  altogether  effaced  during 
the  act  of  inspiration.  (See  figs.  i6i,  162,  163.)  It  is  said 
to  be  always  more  or  less  quickened,  small  and  intermittent  ; 


Fig.  161. —  The  fulsus  paradoxus.     ( After  Ktissmatil.)     Copied  from  Zicii/ssens 
Cyclop(€dia,  vol.  vi.  p.  650. 

'  The  term   indnrative-mcdiastino-pcriiarditis  has  been   given  to  cases  of  this 
description. 


Iitdiirative  Mcdiastino-Pericarditis. 


351 


and   it  may  be  irregular,  while  the  action  of  the  heart  is  at 
the  same  time  perfectly  rhythmical  and  regular.^ 


Fk;.    162.  —  Tlic  pulsus  paradoxus.     (After  Zieiiissen)  Cyclopiedia  of  Medicine^ 

vol.  vi.  p.  656. 


Fig.    163.  —  Tiic  pulsus  pas-adoxns.      (After   Traiihe.)     Copied   from   Zie/nsseii's 
Cydopcedia,  vol.  vi.  p.  654. 

The  obstruction  to  the  passage  of  blood  through  the 
superior  cava  causes  distention  of  the  jugular  veins  ;  and  since 
the  obstruction  only  occurs  during  inspiration,  the  jugular 
veins  become  distended  instead  of  collapsing  during  inspira- 
tion (as  they  do  in  health),  the  distention  rapidly  subsiding 
during  expiration,  that  is,  when  the  constrictive  bands  are 
relaxed,  and  the  obstruction  to  the  blood  in  the  superior 
cava  is  removed. 

Diagnosis. — To  sum  up,  then,  it  is  impossible  in  some 
cases  to  diagnose  an  adherent  pericardium  ;  in  others,  the 
diagnosis  is  difficult ;  while  in  some,  the  condition  can  be 
easily  and  surely  recognised. 

A  history  of  pericarditis  is  presumptive  evidence  of  the 
condition,  for  some  adhesions  usually  remain  after  inflamma- 
tion of  the  pericardial  sac.  Systolic  depression,  instead  of 
systolic  protrusion,  of  the  apex  beat,  is  strongly  suggestive  of 

'  The  pulsus  paradoxus  is  not  pathognomic  of  '  iudiirative-mcdiastinopc7-i- 
carditis,''  though  it  is  strongly  suggestive  of  that  condition — it  has  been  observed 
in  ordinary  pericarditis  without  external  adhesions  ;  also  in  some  cases  in  which  there 
was  an  obstruction  to  the  entrance  of  air  into  the  thorax  (stenosis  of  the  air  passages). 
I  myself  have  seen  a  very  similar  pulse  during  an  attack  of  spasmodic  asthma.  (See 
fig.  103.) 


o:)-' 


Diseases  of  tJie  Heart. 


an  adherent  pericardium  ;  and  the  supposition  is  strength- 
ened by  an  immoveable  apex,  and  an  increased  area  of 
cardiac  dulness  with  fixation  of  the  anterior  margins  of  the 
lungs,  more  especially  of  the  left.  The  diagnosis  is  confirmed 
by  a  permanent  depression  over  the  pr^ecordial  region. 

Systolic  depression  of  the  lower  end  of  the  sternum  and 
adjacent  costal  cartilages,  with  a  diastolic  rebound  of  the 
chest  wall,  and  distention  of  the  veins  of  the  neck  during  the 
systolic  depression  of  the  chest  wall,  followed  by  their  rapid 
collapse  and  disappearance  during  the  diastolic  rebound,  are 
the  strongest  possible  evidence  of  the  condition. 

Indurative-incdiastino-perkarditis  may  be  strongly  sus- 
pected when  the  pulse  presents  the /^/vrc/ai'/m/ character  ;  and 
may  be  positively  diagnosed  when,  in  addition,  there  is  dis- 
tention of  the  cervical  veins  during  inspiration,  followed  by 
their  rapid  collapse  and  disappearance  during  expiration. 

Prognosis.  —  Per  se,  an  adherent  pericardium  is  of  no 
practical  importance  ;  but  since  it  often  leads  to  secondary 
changes  in  the  condition  of  the  heart,  the  prognosis  should 
always  be  guarded,  and  the  case  carefully  watched.  The 
prognosis  entirely  depends,  therefore,  upon  the  effects  which 
the  adherent  pericardium  is  likely  to  have,  or  has  already 
had,  on  the  muscular  walls  and  cavities  of  the  heart,  and 
upon  the  presence  or  absence  of  valvular  complications. 

The  prognosis  is  most  favourable  in  those  cases  in  which 
the  cardiac  muscle  is  sound,  in  which  there  are  no  valvular 
lesions,  and  in  which  the  adhesions  are  not  extensive. 

Extensive  adhesions — evidenced  during  life  by  marked 
systolic  depression  of  the  lower  end  of  the  sternum,  followed 
by  a  notable  diastolic  rebound — lead  in  most  cases,  sooner  or 
later,  to  serious  structural  alterations  in  the  heart.  When  val- 
vular lesions  complicate  the  case,  the  prognosis  is  as  a  rule 
bad  ;  but  there  are  many  exceptions  to  this  general  rule, 
depending  upon  the  nature  and  extent  of  the  valvular  lesion, 
etc.  When  the  myocardium  is  implicated,  the  prognosis  is 
most  unfa\ourablc. 


CJironic  Pericarditis.  353 

Treatiiioit. — Nothing  can  be  done  in  the  way  of  direct 
treatment,  i.e.  removing  the  adhesions.  The  chief  indications 
are  to  maintain  the  general  health  in  the  highest  possible 
state  of  efficiency,  and  in  particular  to  preserve  the  nutrition 
and  strength  of  the  heart ;  to  avoid  all  strain  and  over  exer- 
tion ;  to  treat  the  valvular  complications,  and  to  relieve  symp- 
toms. The  manner  in  which  these  indications  are  to  be 
carried  out  will  be  more  appropriately  considered  when  I 
come  to  treat  of  m\'ocarditis  and  vahular  lesions. 

CHRONIC    PERICARDITIS.^ 

^"Etiology  and  Pathology. — Chronic  inflammation  of  the 
pericardium  is  much  less  frequent  than  the  acute  form  of  the 
affection.  In  some  cases,  the  inflammation  commences  slowl\- 
and  gradually,  in  other  words,  it  is  chronic  from  the  first  ;  in 
others,  an  inflammation  which  was  at  first  acute,  does  not  re- 
solve, but  passes  on  to  the  chronic  condition.  In  both  instances 
there  is  usually  some  cause  of  general  constitutional  depression 
present;  rheumatic  pericarditis  in  a  previously  healthy  person 
very  rarely  assumes  the  chronic  form  ;  the  tubercular  and 
cancerous  forms  of  pericarditis,  on  the  contrary,  are,  as  a  rule, 
subacute  or  chronic.  The  effusion  in  cases  of  chronic  peri- 
carditis is  usually  considerable,  and  often  very  great ;  in  many 
cases  it  is  haemorrhagic  or  purulent  in  character. 

Symptoms  and  physical  signs. — -After  the  full  description 
which  has  been  previously  given,  of  the  symptoms  and  signs 
of  acute  pericarditis,  it  is  unnecessary  to  say  much  with  regard 
to  the  chronic  form.  The  constitutional  depression  is,  as  a 
rule,  more  considerable  than  in  the  acute  variety,  symptoms 
and  signs  of  depression  and  failure  of  the  heart's  action  are,  in 
fact,  amongst  the  most  prominent  features  of  the  case.  When 
the  effusion  is  considerable,  and  when,  as  very  often  happens, 
the  myocardium  is  extensively  affected  by  the  inflammator}- 
process,  symptoms  due  to  mechanical  derangement  of  the 
circulation  and  to  the  pressure  of  the  distended  pericardial 
sac  upon  the  adjacent  organs  and  parts,  are  usually  present. 

'   I  do  not  apply  the  term  chronic  pericarditis,  as  some  writers  do,  to  cases  of 
adherent  pericardium. 

Z 


354  Diseases  of  the  Heart. 

In  some  cases,  the  temperature  is  not  altered,  but  as  a  rule 
there  is  some  increase,  more  especially  of  the  evening  tempera- 
ture. When  the  effusion  consists  of  pus,  ups  and  downs  of 
temperature  with  rigors  and  sweatings  may  occur,  but  these 
alterations  are  perhaps  more  common  during  the  period  of 
pus-formation  than  in  the  after  stages  of  the  case,  i.e.  when 
the  condition  has  become  chronic. 

The  pJiysical  signs  are  the  same  as  those  which  have  been 
described  in  treating  of  acute  pericarditis  with  effusion. 

Diagnosis. — The  diagnosis  is  to  be  arrived  at  in  the  same 
manner  as  has  been  described  in  treating  of  the  diagnosis  of 
acute  pericarditis.  The  differential  distinction  of  chronic  peri- 
cardial effusion,  of  hydropericardium,  and  of  enlargement  of 
the  heart  itself  (more  especially  chronic  pericarditis  and  cardiac 
dilatation),  is  often  extremely  difficult,  but  can  usually  be  made 
by  careful  attention  to  the  points  detailed  in  tables  V.,  VI.,  VII. 
(See  pages  332,  333,  334.) 

Prognosis.- — The  prognosis  of  chronic  pericarditis  is  usually 
unfavourable,  each  case  must,  however,  be  judged  on  its 
own  merits.  The  severity  of  the  symptoms,  the  amount  and 
character  of  the  effusion,  the  exact  nature  of  the  pathological 
condition  (whether  the  pericarditis  'is  rheumatic,  tubercular, 
cancerous,  etc.),  and  the  condition  of  the  other  systems  and 
organs  {i.e.  the  presence  or  absence  of  complications),  are  the 
chief  points  which  should  be  taken  into  consideration. 

Treatment. — The  object  of  treatment  is  to  promote  ab- 
sorption of  the  inflammatory  products,  and  to  restore  the 
pericardium  to  its  natural  condition.  The  means  by  which 
this  end  is  to  be  attained,  have  already  been  described.  (See 
the  headings  4,  5,  and  6,  treatment  of  acute  pericarditis, 
pages  342  to  345.) 

HYDROPERICARDIUM. 

Definitio)i. — The  presence  of  simple  non-inflammatory  fluid 
in  the  pericardial  sac. 

Aitiology. — A  certain  amount,  half  an  ounce  to  two  ounces, 
of  clear  serous  fluid  is  very  commonly  found  in  the  sac  of  the 
pericardium  after  death,  and  is  probably  poured  out  during  the 


Hydropericardiiiiu.  355 

act  of  dying,  or  immediately  after  death.  It  is  only  when  this 
amount  is  considerable,  and  when  the  fluid  is  present  before 
the  act  of  dying  is  established,  that  the  condition  can  properly 
be  termed  hydropericardium.  Dropsy  of  the  pericardium  is 
almost  always  part  and  parcel  of  a  general  dropsy,  and  is 
usually  a  late  event  in  the  course  of  cardiac  or  renal  dis- 
ease ;  but  while  this  is  the  clinical  and  pathological  fact, 
it  cannot  of  course  be  denied  that  hydropericardium  may 
be  local,  and  that  it  may  result  from  an  obstruction  to  the 
return  current  of  blood  from  the  walls  of  the  heart  and  tissues 
of  the  pericardium.  I  have  myself  seen  more  than  one  case 
in  which  the  amount  of  fluid  in  the  pericardium  was  quite  out 
of  proportion  to  the  amount  of  general  dropsy,  and  in  which 
I  have  little  doubt  that  there  was  some  local  cause  for  the 
condition,  such  as  obstruction  of  the  coronary  veins.  Un- 
fortunately the  cases,  which  occurred  some  years  ago,  were 
not  examined  with  the  attention  that  they  deserved,  and  I 
must  content  myself  with  recording  the  bare  fact  of  their 
occurrence. 

Symptojiis. — It  is  seldom  that  the  amount  of  fluid  is  suf- 
ficiently great  to  seriously  interfere  with  the  action  of  the 
heart.  The  symptoms  are,  therefore,  in  most  cases  those  of 
the  primary  condition — cardiac  or  renal  disease  with  dropsy. 
When  the  pericardial  dropsy  is  considerable,  effusion  into  the 
pleural  sacs,  and  other  pulmonary  complications  are,  as  a  rule, 
present.  In  many  cases  there  are  also  other  cardiac  com- 
plications, such  as  valvular  disease,  dilatation,  fatty  degenera- 
tion, etc.  The  physician  must  hesitate,  therefore,  in  ascribing 
the  dyspnoea  and  other  symptoms  of  embarrassed  cardiac 
action,  which  are  generally  prominent  in  cases  of  this  descrip- 
tion, to  the  pericardial  effusion  ;  these  symptoms  are  usually 
for  the  most  part  due  to  other  conditions,  though  the  em- 
barrassment of  the  heart  will  of  course  be  increased  when  the 
pericardial  dropsy  is  great,  and  more  especially  when  a  large 
effusion  is  rapidly  poured  out. 

Physical  sig)is  and  Diagnosis. — The  presence  of  simple 
non-inflammatory  fluid  in  the  sac  of  the  pericardium  is  of 
course  attended   by  an  increase   of  the   praecordial   dulness  ; 


356  Diseases  of  the  Hea  rt. 

the  outline  of  the  duhiess  corresponds  to  that  which  has 
been  described,  in  speaking  of  inflammatory  effusion.  The 
dulness  due  to  simple  dropsy  of  the  pericardium  is  often 
difficult  to  detect,  for,  in  many  cases  it  is  inconsiderable  in 
amount,  and  in  most  cases  the  heart  is  at  the  same  time 
enlarged.  Under  such  circumstances  it  is  very  difficult  or  im- 
possible to  distinguish  the  dulness  derived  from  the  enlarged 
heart  from  the  dulness  due  to  the  pericardial  fluid.  When  the 
pericardial  effusion  is  considerable,  the  cardiac  impulse  and 
cardiac  sounds  may  be  feeble  or  indistinct,  but  the  character 
of  the  impulse  and  of  the  sounds  depends  for  the  most  part 
upon  the  condition  of  the  heart  in  other  respects.  All  that 
can  with  certainty  be  said  is,  that  a  considerable  amount  of 
effusion  will  interfere  with  the  conduction  of  sound,  and  that 
the  cardiac  sounds  (whatever  their  character,  whether  normal 
or  abnormal)  will  probably  be  weaker  than  they  were  before 
the  occurrence  of  the  effusion.  In  other  respects  they  will 
probably  be  unmodified.  Pericardial  friction  is  not  of  course 
present ;  this  fact,  and  the  absence  of  p)-rexia  (unless  some 
inflammatory  complication  should  happen  to  be  present),  to- 
gether with  the  circumstance  that  the  pericardial  effusion  is,  as 
a  rule,  a  late  event  in  the  course  of  general  dropsy,  are  the  chief 
points  on  which  reliance  must  be  placed  in  distinguishing  simple 
non-inflammatory  fluid  in  the  pericardium  from  chronic  peri- 
carditis. I  need  not  go  into  further  details,  but  must  refer  the 
reader  to  table  v.,  p.  332.  I  must,  however,  repeat,  that  the 
diagnosis  of  simple  pericardial  effusion  is  in  most  cases  difficult 
and  sometimes  impossible. 

Prognosis. — The  prognosis  must  be  entirely  guided  by  the 
primary  cause  of  the  condition  ;  it  must,  of  course,  be  remem- 
bered that  dropsy  of  the  pericardium,  sufficient  to  be  recog- 
nised during  life,  seldom  occurs  except  in  the  later  stages  of 
general  dropsy,  and  that  in  cases  of  this  description  {i.e.  cases 
in  which  it  does  occur  in  sufficient  quantity  to  be  recognised) 
the  prognosis  is,  as  a  rule,  most  unfavourable.  An  exception 
occurs  in  some  cases  of  acute  Bright's  disease,  in  which  condi- 
tion the  prognosis  is  much  more  favourable. 

Treatment. — The  treatment  must,  for  the    most   part,  be 


Pncii  mopcrica  rdiu  in .  357 

directed  to  the  primary  condition  (the  cardiac  or  renal  disease) 
on  which  the  pericardial  effusion  depends.  The  general  treat- 
ment is  in  fact  that  of  an  advanced  case  of  cardiac  or  renal 
dropsy.  Digitalis,  purgatives,  etc.,  in  those  cases  in  which 
there  is  evidence  of  localised  venous  engorgement  and  over- 
distention  of  the  right  heart,  local  or  even  general  venesection, 
are  the  most  useful  measures  which  can  be  employed.  Counter 
irritation  (iodine,  blisters)  over  the  pericardium  is  sometimes 
useful.  When  the  effusion  is  very  great,  and  more  especially 
when  it  is  poured  out  with  sufficient  rapidity  to  seriously  em- 
barrass the  action  of  the  heart,  paracentesis  pericardii  is  advis- 
able; no  case  of  this  description  has  come  under  my  own 
observation. 

PNEUMOPERICARDIUM. 

Definition. — The  presence  of  gas  in  the  bag  of  the  peri- 
cardium. 

^Etiology  (iJid  Pathology.  —  Pneumopericardium  is  ex- 
tremely rare.  The  gas  almost  invariably  enters  the  peri- 
cardium from  without,  occasionally  as  the  result  of  wounds  of 
the  chest  wall  (stabs,  the  operation  of  paracentesis  pericardii) 
more  frequently  in  consequence  of  a  communication  being 
established,  as  the  result  of  disease,  between  the  sac  of  the 
pericardium  and  some  of  the  surrounding  air-containing 
viscera  (the  oesophagus,  lungs,  stomach).  It  has  also  been 
supposed  that  gas  may  be  secreted  by  the  lining  membrane 
of  the  pericardium,  or,  may  be  produced  as  the  result  of  the 
decomposition  of  inflammatory  (purulent)  fluid  within  the  sac. 
It  is  not  at  all  uncommon  in  advanced  states  of  decomposi- 
tion to  meet  with  foetid  gas  in  the  sac  of  the  pericardium  after 
death,  but  these  cases,  which  must  of  course  be  carefully  dis- 
tinguished from  true  pneumopericardium,  do  not  support  the 
occurrence  of  decomposition  during  life.  Pneumopericardium 
is  (?)  always  associated  with  pericarditis,  and  since  the  inflam- 
matory products  are  almost  always  purulent,  pneumopericar- 
dium is  practically  synonymous  with  the  condition  to  which 
the  term  pyo-pncmnopcricardinin  has  been  applied. 

Symptoms  and  physical  signs. — The  symptoms  are  those 
of  pericarditis,  usually  of   purulent    pericarditis.      In    many 


358  Diseases  of  the  Heart. 

cases  symptoms  and  signs  of  disease  in  the  surrounding 
viscera  (cancer  of  the  oesophagus,  abscess  in  the  hver,  disease 
of  the  lung,  etc.)  are  also  present.  The  physical  signs  are 
characteristic  of  the  presence  of  gas  and  fluid.  The  percussion 
note  is  tympanitic  over  the  position  of  the  gas  ;  and  it  is 
needless  to  say  that  this  varies  with  the  position  of  the  patient, 
since,  when  gas  and  fluid  are  both  present,  the  fluid  necessarily 
gravitates  to  the  lower  level.  On  auscultation,  splashing,  gurg- 
ling, churning  sounds,  often  of  a  metallic  pitch,  and  sometimes 
auto-audible,  which  correspond  in  rhythm  to  the  cardiac  con- 
tractions, are  heard. 

Diagnosis. — The  diagnosis  docs  not,  as  a  rule,  present 
any  difficulties ;  the  condition  must,  of  course,  be  distinguished 
from  others  in  which  a  cavity  containing  air  and  fluid  is  in 
close  contact  with  the  heart  (pneumo-thorax,  a  cavity  in  the 
lung,  and  a  distended  stomach),  the  position  of  the  reson- 
ance (over  the  centre  of  the  heart  when  the  patient  lies  on  his 
back),  the  fact  that  the  splashing  sounds  are  synchronous 
with  the  cardiac  contractions,  the  nature  of  the  symptoms,  and 
the  character  of  the  associated  physical  signs,  could  hardh' 
fail  to  enable  a  careful  observer  to  come  to  a  correct  conclusion 
as  to  the  nature  of  the  case. 

Prognosis. — The  prognosis  is  very  unfavourable,  though 
not  so  hopeless  as  might  a  priori  be  supposed.  The  nature 
of  the  primary  affection  is  one  of  the  most  important  elements 
to  be  taken  into  consideration  in  attempting  to  determine  the 
future  course  of  the  case.  When  the  condition  is  due  to 
traumatic  injury,  the  prognosis  is  more  hopeful  than  in  any 
other  form  ;  when,  on  the  contrary,  the  condition  results,  as  it 
did  in  the  case  related  by  Begbie,^  from  the  perforation  of  a 
cancerous  tumour  of  the  oesophagus,  the  prognosis  is  of  course 
hopeless.  Each  case  must  therefore  be  judged  on  its  own 
merits,  special  attention  being  given  to  the  aetiology  and  the 
points  which  guide  the  physician  in  forming  a  prognosis  in 
purulent  pericarditis. 

Treatment. — The  same  treatment  which  has  been  recom- 
mended for  purulent  pericarditis  must  be  carried  out.     With 

'  Edbtlnirgh  Medical  Journal,  1S62. 


Hcnnoper'icardiinn.  359 

rare  exceptions,  such,  for  instance,  as  pneumopericardium  the 
result  of  cancerous  perforation,  the  sac  of  the  pericardium 
should  be  laid  open  and  a  drainage  tube  inserted,  the  strictest 
antiseptic  precautions  being  of  course  observed,  during  the 
operation  and  the  subsequent  progress  of  the  case. 

H^MOPERICARDIUM. 

When  pure  blood  is  found  in  the  cavity  of  the  pericardium 
after  death,  it  has  usually  escaped  either  from  a  rupture  in  the 
heart  itself,  from  an  aortic  aneurism,  or  from  a  rupture  of  the 
coronary  artery.  The  s)'mptoms  and  physical  signs  which 
chafacterise  cases  of  this  description  are  detailed  in  other 
parts  of  this  work.  (See  spontaneous  rupture  of  the  heart, 
aneurism  of  the  thoracic  aorta.) 

Those  cases  of  pericarditis  in  which  the  inflammatory, 
exudation  is  bloody,  have  been  already  referred  to.  (Sec  page 
301O 


360  Diseases  of  the  Heart. 


CHAPTER    V. 

THE  DISEASES  OF  THE  ENDOCARDIUM.  ACUTE  SIMPLE  ENDOCARDITIS. 
ULCERATIVE  ENDOCARDITIS.  CHRONIC  ENDOCARDITIS.  CHRONIC 
VALVULAR  LESIONS.  MITRAL  INCOMPETENCE.  MITRAL  STENOSLS. 
AORTIC  INCOMPETENCE.  AORTIC  STENOSIS.  TRICUSPID  INCOM- 
PETENCE. TRICUSPID  STENOSIS.  PULMONARY  STENOSIS.  PUL- 
MONARY INCOMPETENCE. 

The  endocardium,  or  membrane  which  lines  the  interioi 
of  the  heart,  and  which,  at  the  auriculo-ventricular  and 
arterial  orifices  is  folded  on  itself  so  as  to  form  the  valve 
sci^ments  (auriculo-ventricular  and  sigmoid  ^  valves)  is  liable 
to  be  affected  by  acute  inflammation  and  by  chronic  inflam- 
matory and  degenerative  processes.  All  of  these  conditions 
are  of  great  practical  importance,  more  particularly  from  the 
fact  that  they  are  the  most  common  and  important  causes  of 
cardiac  valvular  lesions. 

In  studying  the  diseases  of  the  endocardium  the  following 
facts  should  be  remembered  : — 

1.  That  these  affections  are  seldom  primary. 

2.  That  the  valve  segments  and  chordae  tendineas  are  the 
parts  of  the  endocardium  on  which  the  stress  of  the  lesion, 
so  to  speak,  falls.- 

■  The  endocardial  or  inner  lining  membrane  of  the  heart  is  prolonged  over  the 
sigmoid  (aortic  and  pulmonary)  valves,  and  becomes  continuous  with  the  inner 
coat  of  the  artery. 

'"'  The  valve  segments  are  often  the  only  parts  of  the  endocardium  (to  the 
naked  eye  at  least),  which  appear  diseased,  and  in  almost  all  cases  they  are  the 
parts  which  are  first  and  most  affected.  The  greater  tendency  which  diseased 
processes  have  to  locate  themselves  on  the  valves,  is  probably  due  to  the  fact  that 
the  valvular  segments  are  the  parts  of  the  endocardium  which  are  most  exposed 
to  mechanical  irritation  and  shock,  but  to  this  point  I  will  again  refer  in  speaking 
of  the  tendency  of  particular  parts  of  the  valve  to  be  affected  by  acute  inflamma- 
tion. 


Aaite  Endocarditis.  361 

3.  That  after  birth  the  affections  of  the  endocardium  are 
usually  left  sided.^ 

Let  us  now  consider  the  affections  of  the  endocardium  in 
detail. 

ACUTE   ENDOCARDITIS. 

Definition. — Acute  inflammation  of  the  endocardium. 

Varieties. — Several  different  varieties  of  acute  endocarditis 
have  been  described,  but  for  practical  purposes  two  chief 
pathological  forms  are,  I  think,  sufficient,  viz. : — 

I.'  Acute  simple  endocarditis. 

2.  Acute  ulcerative  endocarditis.^ 

ACUTE   SIMPLE   ENDOCARDITIS. 

JEtioIogy. — The  causes  of  acute  simple  endocarditis  are 
very  similar  to  the  causes  of  acute  pericarditis. 

The  condition  is  almost  always  secondary,  a  large  propor- 
tion of  the  cases  being  rJicnniatic  (occurring  more  particularly 
in  the  course  of  acute  and  subacute  articular  rheumatism). 
Scarlet  fever  is  another  affection,  which,  as  Dr  Sansom  more 
particularly  has  insisted  upon,  is  often  associated  with  or 
followed  by  endocarditis.  Inflammation  of  the  endocardium 
is  met  with  in  a  considerable  number  of  cases  of  chorea,^  it 
also  occasionally  occurs  in  connection  with  measles,  puerperal 
fever,  pyaemia,  diphtheria,  typhoid,  etc. 

'  Various  theories  have  been  put  forward  to  account  for  the  fact  that  the  left 
endocardium  is  so  much  more  frequently  affected  by  disease  than  the  right.  It 
has  been  supposed,  for  example,  that  the  different  character  of  the  blood  in  the 
two  hearts  was  the  cause  of  the  condition  ;  the  left  heart,  which  contains  arterial 
blood,  being,  it  is  theorised,  more  liable  to  inflammatory  changes  than  the  right 
heart,  which  contains  venous  blood.  A  more  probable  explanation  is  that  which 
accounts  for  the  condition  by  the  fact,  that  the  valves  of  the  left  heart  are  more 
exposed  to  irritation  and  shock,  in  consequence  of  their  being  more  forcibly  and 
violently  closed,  than  those  of  the  right. 

^  It  is  a  disputed  point  whether  there  is  any  essential  and  primary  difference 
between  these  two  forms.  Some  authorities  say  that  it  is  the  constitutional  con- 
dition, of  the  individual  who  is  affected  by  the  endocardial  inflammation,  which 
determines  the  form  of  the  lesion  (whether  simple  or  ulcerative)  rather  than  any 
essential  difference  in  the  nature  of  the  inflammatory  process. 

'  In  many  cases  of  chorea  the  endocarditis  is  also  rheumatic. 


362  Diseases  of  the  Heart, 

Authorities  differ  as  to  the  exact  frequency  with  which 
endocarditis  occurs  in  rheumatic  fever.  Most  Enghsh  and 
French  observers  place  the  proportion  as  high  as  one  in  two 
or  three,  while  many  German  physicians  make  it  as  low  as 
one  in  five  or  six.^  The  discrepancy  is  probably  due  to  the 
fact  that  observers  are  not  agreed  as  to  the  clinical  indica- 
tions of  endocarditis  during  life. 

Opinions  also  differ  as  to  the  influence  which  the  severity 
of  the  attack  of  rheumatic  fever  has  in  producing  the  endo- 
cardial mischief  Some  authorities,  Sibson-  for  example, 
state  that  the  more  severe  the  rheumatic  attack,  the  greater 
the  tendency  to  endocardial  inflammation.  Others,  such  as 
Sansom,  have  not  observed  any  such  relationship  ;  Sansom, 
indeed,  believes  '  that  in  the  child  endocarditis  can  arise  and 
progress  without  special  symptoms,  without  pyrexia,  without 
the  disturbing  influence  of  any  acute  disease,'  ^  and  he  states 
that  this  form  of  endocarditis  presents  '  no  obvious  difference 
from  the  essential  features  of  rheumatic  endocarditis,  such  as 
we  find  in  the  undoubtedly  rheumatic  subjects.'  ^ 

Inflammation  of  the  endocardium  should  not  be  looked 
upon  as  a  complication  but  as  a  component  part  of  articular 
rheumatism  ;  it  may  occur  at  any  period  of  an  attack,  and 
may  even  precede  the  joint  affection.  In  many  cases  the 
two  conditions  (the  joint  affection  and  the  endocarditis)  are 
probably  developed  simultaneously.  In  the  cases  observed 
by  Sibson,  a  systolic  mitral  murmur,  which  he  considered  a 
certain  sign  of  endocarditis,  was  present  in  one-fourth  before 
the  end  of  the  first  week,  and  in  two-thirds  before  the  end  of 
the  second  week  ;  and  it  is  important  in  this  connection  to 
remember  that  the  endocardial  inflammation  must  have  been 
going  on  for  some  time  before  the  systolic  murmur  was 
observed,  for  considerable  changes  must  be  produced  in  the 

'  Sibson  states  that  endocarditis,  either  alone  or  in  the  form  of  endo-peri- 
carditis,  was  present  in  half  of  the  325  cases  of  acute  rheumatism  which  were  under 
his  care  in  St  Mary's  Hospital  during  the  years  185 1  to  1866,  and  that  in  one- 
half  of  the  remainder  the  occurrence  of  endocarditis  was  either  threatened  or 
probable. — Russell  Reynolds'  System  0/ Medicine,  vol.  iv.  p.  526. 

^  Russell  Reynolds,  vol.  iv.  p.  199. 

'  Lettsomian  Lectures,  p.  23.  ■*  Loc,  Cit.,  p.  23. 


yE  Ho  logy  of  Aaite  Simple  Endocarditis.      363 

valve  segments  or  myocardium  before  incompetence  is  estab- 
lished ;^  in  other  words,  the  systoHc  apex  murmur  indicative 
of  mitral  regurgitation,  and  which  is  the  chief  clinical  sign 
of  endocarditis,  is  not  developed  immediately  the  valvular 
inflammation  is  established. 

Amongst  the  predisposing  causes,  previous  attacks  of 
endocarditis,  the  presence  of  structural  alterations  in  the 
valves,  the  result  of  previous  endocarditis  and  of  chronic 
degenerative  changes,  and  any  alterations  (such  as  congenital 
malformations)  which  expose  the  valves  to  a  greater  amount 
of  mechanical  irritation  and  shock  than  they  are  normally 
subjected  to,  must  be  mentioned. 

After  puberty  the  two  sexes  are  equally  predisposed  to 
acute  endocarditis.^  Children  seem  more  liable  to  be  affected 
than  adults.^  Anything  which  debilitates  the  system  as  a 
whole  (such  as  poverty,  exposure,  etc.),  more  especially  any- 
thing which  predisposes  to  acute  articular  rheumatism,  predis- 
poses to  the  condition.  A  hereditary  tendency  to  rheumatism 
must  therefore  be  mentioned  as  a  predisposing  cause. 

Pathology  and  Morbid  Anatomy.— ■  KcvXq  simple  endo- 
carditis is  almost  always  secondary.  It  is,  in  the  majority 
of  cases,  so  far  as  we  can  judge  by  the  naked  eye,  limited 
to  the    valvular    apparatus  of  the    left    heart,    though   acute 

'  Sibson  indeed  goes  so  far  as  to  say,  '  we  are  therefore,  I  conceive,  warranted 
in  assuming  that  in  a  considerable  number  of  cases,  the  active  stage  of  the  endo- 
carditis is  passing  away  at  the  lime  of  the  appearance  of  the  murmur.' — Russell 
Reynolds'  System  of  Medicitte,  vol.  iv.  p.  475. 

^  The  preliminary  report  of  the  Collective  Investigation  Committee  of  the 
British  Medical  Association  seems  to  show  that  'between  the  ages  of  eleven  and 
fifteen,  acute  rheumatism  is  three  times  more  frequent  among  females  than  males  ; 
between  sixteen  and  twenty  the  numbers  are  practically  equal ;  while,  after  this  age, 
the  disease  is  far  more  frequent  among  males  than  females  up  to  the  age  of  forty- 
five,  when  they  again  become  equal.' — The  Collective  Investigation  Record,  p.  121. 
The  fact  that  young  females  suffer  so  much  more  frequently  from  acute  rheumatism 
than  young  males,  is  probably  the  reason  why  they  are  so  much  more  frequently 
affected  with  mitral  stenosis.  Possibly,  too,  as  Dr  Barlow  has  suggested,  the 
greater  liability  of  female  children  to  chorea,  in  which  endocarditis  is  of  common 
occurrence,  is  another  reason  why  mitral  stenosis  occurs  more  frequently  in  women. 

'  Rosenstein  differs  from  most  authorities  on  this  point,  for  he  considers  '  the 
disposition  to  endocardial  affections,  on  the  whole,  smaller  in  childhood  than 
after  puberty.' — Ziemssen' s  Cyclopcedia  of  Medicine,  vol.  vi.  p.  85. 


364  Diseases  of  tJie  Heart. 

endocarditis  of  the  valvular  apparatus  of  the  right  heart,  more 
especially  of  the  tricuspid  valve,  is,  I  believe,  more  common 
than  is  generally  supposed.  (Like  the  acute  endocarditis 
of  chorea,  right-sided  endocarditis  is,  I  think,  in  many  cases 
completely  curable.)  The  mitral  valve  is  more  frequently 
affected  than  the  aortic,  a  fact  which  Sibson  states  is  due  to 
the  circumstances  'that  the  mitral  flaps  press  against  each 
other  when  the  valve  is  shut,  with  much  greater  tension,  force, 
and  concentration,  than  the  margin  of  contact  of  the  aortic 
valve,  under  the  triple  agency  of  a  finer  margin  of  contact, 
greater  pressure  of  blood  and  the  muscular  force  and  tendin- 
ous traction  proper  to  the  valve.' ^  The  chordae  tendineae  are 
frequently  implicated.  In  a  few  cases  the  endocardium, 
lining  the  cavities  of  the  left  auricle  and  left  ventricle  is 
involved.  It  is  quite  exceptional  to  find  the  inflammation 
limited  to  the  right  heart." 

In  the  earliest  stages  of  the  process,  which  we  compara- 
tively seldom  have  an  opportunity  of  observing  after  death, 
little  nodulated  swellings  of  a  rosy  tint  and  jelly-like  consist- 
ence are  seen  at  the  margins  of  the  affected  segments,  more 
especially  on  the  auricular  surface  of  the  mitral  and  on  the  ven- 
tricular surface  of  the  aortic  valve  around  the  corpora  Arantii. 
Should  the  endocardium  lining  the  cavities  of  the  heart  be 
involved,  the  affected  portion  of  the  membrane  seems  to  have 
lost  its  polish  and  to  be  somewhat  opaque  ;  and  distended 
blood  vessels  can  sometimes  be  observed  coursing  over,  or 
more  correctly  under,  the  affected  portion  of  the  membrane.^ 

A  little  later  the  vegetations,  which  are  the  most  character- 
istic and  striking  morbid  appearances  of  acute  endocarditis, 
are  observed.  Now,  since  the  inflammatory  changes  are 
always  first  and  most  marked  on  those  portions  of  the  valves, 

'  Russell  Rtynolds'  System  of  Medicine,  vol.  iv.  p.  458. 

■  This  statement  does  not  of  course  apply  to  the  foetus  and  newly  born  child, 
in  whom  the  right  endocardium  is  much  more  frequently  involved  than  the  left. 

^  Capillary  blood-vessels  are  'numerous  in  the  pericardial  and  endocardial 
membrane,  including  the  valves'  (Klein  and  Noble  Smith,  Atlas  of  Histology, 
page  148) ;  and  vessels  of  some  size  are  met  with  here  and  there  just  beneath  the 
endocardium,  i.e.  between  the  endocardium  and  myocardium  in  the  sub-endo- 
cardial  connective  tissue. 


Pathology  of  Acute  Simple  Endocarditis.      36; 


which  are  most  exposed  to  friction  and  pressure,  the  vegeta- 
tions are  generally  first  seen  on  the  auricular  surface  of  the 
mitral  and  on  the  ventricular  surface  of  the  aortic  segments, 
not,  it  must  be  noted,  on  the  free  edges  of  the  valve,  but  on 
the  lines  of  maxiimnn  contact,  which,  as  Sibson  has  shown,  are 
not  the  free  margins,  but  those  portions  of  the  auricular 
surfaces  of  the  mitral  and  of  the  ventricular  surfaces  of  the 
aortic  segments  which  are  situated  just  within  the  free 
margins.^      (See  figs.    164  and    165.)      The    position    of   the 


Fig.   164.  Fig.   165. 

Fig.  164. — Early  endocarditis  of  the  aortic  ;  and  FlG.  \6^,  of  tlic  7nitral  vahe. 

—  [After  Green.) 

a,  a,  bead-like  fringe  of  vegetations. 

vegetations  on  the  valves  is  probably  also  to  some  extent 
determined  by  the  distribution  of  the  blood-vessels.  When 
the  endocardium,  covering  the  chordae  tendinese  or  walls  of 
the  heart,  is  implicated,  vegetation  may  of  course  also  be  seen 
in  these  situations. 

At  first  the  vegetations  are  of  small  size,  and  give  the 
affected  portion  of  the  membrane  a  beaded  or  roughened 
appearance, — as  the  case  progresses  they  may  become  larger, 
and  sometimes  attain  to  considerable  dimensions,  forming  fun- 
gating  projections  which  may  be  sufficiently  large  to  produce 
considerable  obstruction  of  the  valvular  orifice.'-^    (See  fig.  166.) 

'  That  mechanical  causes  exert  a  very  decided  influence  in  determining  the 
maximum  position  of  the  inflammation,  vegetations,  etc.,  is  very  clearly  seen  in 
some  cases  of  fungating  and  ulcerative  endocarditis, — as  Wilks  and  jMoxon,  and 
many  other  observers  have  insisted  upon.     (See  figure  i6S. ) 

■  Fungating  vegetations  of  this  description  are  more  common  in  the  ulcerative 
than  in  the  simple  form  of  the  disease. 


366  Diseases  of  the  Heart 

When  the  chordae  tendineae  are  swollen  and  covered  with 
vegetations,  they  very  much  resemble  in  shape  ears  of  corn. 
(See  fig.  166.) 

Portions  of  the  vegetations  are  not  unfrequently  detached 
and  carried  by  the  blood  current  to  distant  organs,  producing 
characteristic  embolic  symptoms. 

The  subsequent  changes  vary  considerably  in  different 
cases.  In  the  majority,  there  is  more  or  less  absorption  of  the 
inflammatory  products,  and  cicatricial  contraction  and  harden- 
ing of  the  aiTected  tissues  occur.  This  process  of  healing  is 
however,  very  apt  to  be  attended  with  disastrous  results,  for 
in  consequence  of  the  cicatricial  contraction  the  normal 
relationship,  of  the  valve  segments  to  the  valvular  orifices,  is 
more  or  less  interfered  with,  and  valvular  incompetence  or 
valvular  obstruction,  or  both  conditions,  very  frequently 
remain.  Acute  endocarditis,  in  short,  is  very  often  the 
immediate  and  direct  cause  of  chronic  valvular  lesions.  In 
some  cases  the  inflamed  segments  become  adherent  to  one 
another  or  (very  exceptionally)  to  the  walls  of  the  heart  ; 
and  this  is  another  way  in  which  valvular  stenosis  or  valvular 
incompetence  may  be  established.  Sometimes  the  inflamed 
and  softened  parts  yield  to  the  blood  pressure.  Valvular 
aneurisms,  valvular  ruptures,  or  ruptures  of  the  chordae  ten- 
dineae may  follow.     (See  figs.  169,  170,  and  171.) 

The  mia'oscopical  appearances  of  endocarditis. — A  section 
through  the  normal  endocardium  is  composed  of  the  follow- 
ing parts : — 

1.  A  layer  of  flat  endothelium  cells.     (See  fig.  167.) 

2.  A  layer  of  branched  connective  tissue  cells,  and  a  dense 
net-work  of  elastic  fibres. 

3.  A  layer  of  fibrous  and  elastic  connective  tissue  arranged 
in  the  form  of  trabeculae.  The  thickness  of  this  layer  varies 
considerably  in  dififerent  parts  of  the  heart.  It  is  much 
thicker  in  the  auricles  (more  especially  the  left  auricle)  than 
in  the  ventricles,  and  is  doubtless  intended  to  strengthen  the 
comparatively  weak  muscular  wall  of  the  auricles,  and  to 
resist  the  blood  pressure.  The  outer  fibrous  layer  is  directly 
continuous  with  the  sub-endocardial  connective  tissue,  which 


Fig.  166.      Vegetations  un  t/ie  Mitral  Valve.     (^Xatural  size.) 

+V,  ^  -l^'f®  T^^  °^  ^^^  vegetations  (a)  is  attached  to  tlie  free  margiji  of  the  anterior  segment  of 
the  mitral  valve  ;  many  of  the  chord®  tendineae  (6)  are  thickened  and  roughened  bv  deposits  of 
nDrine.  A  piece  of  white  paper  has  been  placed  in  the  mitral  orifice,  i.e.  behind^the  anterior 
cusp.     Ihe  letter  c  points  to  the  base  of  the  aorta  and  aortic  valve  cusps;  d,  d,  papillary 


Pathology  of  Acute  Simple  Endocarditis.      367 

in  its  turn  is  continuous   with   the  connective   tissue  of  the 
myocardium. 

In  the  sub-endocardial  connective  tissue  blood-vessels  are 
situated.  Fat  cells,  and  unstriped  muscular  fibres  are  also 
seen  beneath  the  endocardium  in  certain  parts  of  the  heart. 


Fig.  167. — Section  thnnioh  the  normal  cndocaniittni.— {After  Qiiain.) 

a,  Lining  epithelium  ;  /^,  connective  tissue  with  fine  elastic  fibres  ;  c,  layer  with 
coarser  elastic  fibres ;  d,  subendo-cardial  connective  tissue  continuous  with  the 
intermuscular  tissue  of  the  myocardium  ;  /i,  muscular  fibres  of  the  myocardium  ; 
w,  plain  muscular  tissue  in  the  endocardium. 

The  valves  are  simply  folds  of  the  endocardium  separated 
by  more  or  less  connective  tissue.  (See  figs.  181,  182,  and 
183.)  The  chordae  tendineae  of  the  mitral  valve  are  attached 
to  the  fibrous  layer  on  the  ventricular  surface  of  the  valve. 

Now  in  acute  endocarditis  the  following  changes  are 
observed  : — 

1.  Proliferation  of  the  endothelial  layer.  This  change  is 
seldom  seen,  but  in  favourable  sections,  made  in  the  earliest 
stages  of  the  affection,  it  could  probably  be  demonstrated. 

2.  Proliferation  of  the  branched  cells  of  the  second  layer. 
This  is  one  of  the  most  striking  features  of  acute  endocarditis, 
and  it  is  to  the  proliferation  of  the  cells  of  this  layer  that  the 
swollen  appearance  of  the  valves  is  in  great  part  due. 

3.  Infiltration  of  the  whole  thickness  of  the  valves  with 
leucocytes,  and  proliferation  of  the  connective  tissue  corpuscles. 

4.  A  deposit  of  fibrine,  in  the  meshes  of  which  leucocytes 
become  entangled,  on  the  surface  of  the  inflamed  part. 

The  vegetations,  which  are  the  characteristic  naked  eye 
features  of  acute  endocarditis,  are  therefore  seen  to  be  com- 
posed of  an  organised  base  formed  by  the  cellular  proliferation 


368  Diseases  of  t lie  Heart. 

of  the  second  layer,  on  the  top  of  which  a  deposit  of  fibrine 
has  taken  place. 

During-  the  process  of  absorption  and  cicatrisation  many 
of  the  cellular  elements  disappear  ;  others  become  elongated 
and  spindle-shaped,  and  are  ultimately  converted  into  fibrous 
tissue  ;  the  whole  tissue  becomes  dense  and  firm,  and  cal- 
careous particles  are  often  deposited  at  the  seat  of  the  lesion. 

In  a  considerable  number  of  cases,  endocarditis  is  com- 
bined with  pericarditis  ;  the  naked  eye  and  microscopical  ap- 
pearances, characteristic  of  inflammation  of  the  pericardium 
are  then  of  course  seen. 

Inflammation  of  the  endocardium  does  not  seem  to  have 
the  same  tendency  to  produce  serious  myocarditis  as  inflam- 
mation of  the  pericardium  has  ;  nevertheless  the  two  condi- 
tions (endocarditis  and  myocarditis)  are  not  unfrequcnth- 
associated  ;  and  in  severe  cases  of  endocarditis  the  layer  of 
muscular  fibres  next  the  endocardium  is  general!}'-  involved. 
In  almost  all  cases  there  is  some  inflammatory  infiltration  of 
the  fibrous  septa  and  lymphatic  spaces  between  the  muscular 
fibres  adjacent  to  the  inflamed  membrane.  When  the  chordae 
tendineffi  are  affected,  the  papillary  muscles  may  become 
seriously  implicated. 

The  Clinical  History  of  Acute  Simple  Endocarditis. 

Symptoms. — In  a  large  proportion  of  cases,  acute  simple 
endocarditis  (when  uncomplicated  with  pericarditis  or  myo- 
carditis)  is   entirely    unattended    by  cardiac   .symptoms,^  the 

'  The  statement  in  the  text  which  represents  my  own  experience,  accords  with 
that  of  most  authorities.  It  is  important,  however,  to  mention  that  Sibson  differs 
from  the  generally  received  opinion.  He  states,  '  in  nearly  every  case  of  endo- 
carditis the  patient  presents  great  or  considerable  general  illness.  Thus  in  sixty-two 
of  the  seventy-one  cases  of  mitral  endocarditis  the  illness  was  great  or  considerable, 
in  two  it  was  definite,  and  in  five  it  was  slight  ;  while  in  two  there  is  no  description 
of  the  general  state  of  the  patient.'  .  .  .  '  Those  cases  in  which  there  was  no 
endocarditis,  present  a  very  different  aspect,  since  in  scarcely  one-third  of  them  was 
there  considerable  general  illness.'  .  .  .  'The  illness  in  cases  of  endocarditis 
is  peculiar.  It  differs  from  and  is  superadded  to  that  due  to  simple  rheumatic 
inflammation  of  the  joints,  and  is  such  as  to  call  the  attention  of  the  physician  to 
the  state  of  the  heart.  The  face  may  be  flushed  all  over,  the  forehead,  nose,  lips 
and  chin  being  of  as  high  a  colour  as  the  cheeks,  a  state  that  is  usually  associated 


Syuiptovis  of  Acute  Endocarditis.  369 

clinical  picture  being  made  up  of  the  symptoms  due  to  the 
primary  disease.  In  the  course  of  acute  rheumatism,  for 
example,  acute  endocarditis  may  become  developed,  and 
may  run  its  course  without  any  prsecordial,  pain,  palpitation, 
or  distress,  without,  in  short,  any  subjective  cardiac  sensa- 
tions being  complained  of,  and  without  any  evident  mechanical 
derangement  of  the  circulation.  The  pulse  and  temperature, 
which  are  of  course  always  more  or  less  affected  by  the 
rheumatic  attack,  may  present  no  characteristic  modifications. 
The  patient  may  recover  frorri  the  rheumatic  fever,  totally 
unconscious  that  his  heart  has  been  seriously  involved  ;  and 
it  is  perhaps  only  when  the  symptoms  of  a  valvular  lesion  are 
subsequently,  and  perhaps  a  long  time  afterwards,  developed, 
that  the  occurrence  of  rheumatic  endocarditis  is  suspected. 
These  are  the  cases  of  so  called  latent  endocarditis. 

In  a  second  group  of  cases,  there  is  more  or  less  precordial 
uneasiness  and  palpitation  ;  with  the  onset  of  the  endocardial 
inflammation,  the  pulse  becomes  quicker  and  more  irritable, 
and  the  pyrexia  already  present,  as  the  result  of  the  rheumatic 
condition,  may  become  distinctly  increased.  There  are  in 
short  some  subjective  cardiac  sensations,  but  no  symptoms 
due  to  mechanical  derangement  of  the  circulation.  A  large 
proportion  of  cases  comes  under  this  head. 

with  profuse  perspiration,  drops  of  sweat  standing  in  beads  on  the  surface — a 
condition,  however,  that  may  be  present  in  cases  with  severe  affection  of  the  joints 
without  endocarditis.  Thus  when  endocarditis  exists,  the  face  loses  the 
i)rightness,  glow,  and  smoothness,  and  the  variety  of  hue  and  tone  of  health,  and 
becomes  clouded,  being  dusky,  dull,  or  ashy  in  hue,  or  glazed,  or  unduly  white, 
or  even  of  a  bluish  tint.  The  countenance,  no  longer  expressive  of  interest  in 
things  and  persons  around,  or  even  of  pain  in  the  limbs,  is  marked  by  internal 
trouble.  The  aspect  of  the  patient  is  altered,  often  profoundly  so,  being  anxious, 
depressed,  or  indifferent.     The  eye  loses  its  lustre  and  expression,  and  becomes 

heavy  and  dull The  breathing  is  usually  affected,  being  more  or  less 

(|uickened Pain  in  the  region  of  the  heart,  sometimes  severe  and 

lasting,  sometimes  slight  or  transient,  amounting  perhaps  only  to  uneasiness,  was 
jiresent  in  about  one-fourth  of  the  cases  of  tricuspid  and  mitral  murmur  belonging 
to  the  earlier  series,  and  in  one-half  of  the  later  series  treated  by  rest.' — Russell 
Reynolds,  vol.  iv.  p.  471. 

The  reader  is  referred  to  the  original  for  a  full  descrijotion  of  the  symptoms, 
which  Sibson  thinks  are  characteristic,  space  only  allows  me  to  give  the  more 
important,  and  those  which  were  most  frequently  present. 

A  A 


370  Diseases  of  the  Heart. 

In  a  third  group,  the  endocarditis  may  be  latent,  or  the 
symptoms  characteristic  of  the  second  group  of  cases  may  be 
present,  when  symptoms  indicative  of  emboHc  plugging  of 
some  distant  vessels  (such,  for  example,  as  right  hemiplegia 
with  aphasia)  suddenly  occur,  and  at  once  direct  attention  to 
the  heart. 

In  7K  fourth  group  of  cases  cardiac  symptoms  (both  subjec- 
tive cardiac  sensations  and  symptoms  due  to  mechanical 
derangement  of  the  cardiac  pump)  are  prominent.  I  must 
repeat,  however,  that  the  cases  included  in  this  group  con- 
stitute a  minority,  probably  a  small  minority  of  the  whole.^ 
In  this  group  are  included  those  cases  in  which  :  — 

(a)  The  valvular  lesion  resulting  from  the  endocarditis  is 
so  severe  as  to  seriously  interfere  with  the  normal  course  of 
the  circulation  during  the  acute  stage  of  the  attack  ;  as,  for 
instance,  where  ulceration  or  rupture  of  a  valve  segment 
occurs,  or  where  the  vegetations  are  produced  in  such  exuber- 
ance as  to  seriously  obstruct  the  valvular  orifice ;-  or  where 
thrombi  are  formed  in  the  cardiac  cavities. 

(b)  Acute  endocarditis  attacks  a  valve  which  is  already  in 
a  state  of  disease,  upsetting  the  balance  of  compensation,  and 
producing  serious  symptoms. 

In  treating  of  the  general  pathology  of  cardiac  affections, 
1  laid  particular  stress  upon  the  fact,  that  so  long  as  the  val- 
vular lesion  is  compensated  by  secondary  hypertrophy,  cardiac 
symptoms  are  usually  slight  or  wanting.  It  must,  however, 
be  remembered,  that  in  cases  of  this  description  the  heart  is 
working  up  to  its  full  power  ;  it  has,  as  it  were,  little  or  no 
reserve  force  with  which  to  meet  sudden  emergencies  ;  under 
such  circumstances  an  endocarditis,  which  in  a  healthy  person 
{i.e.  a  person  whose  heart  was  previously  healthy)  would  be 
unattended  b}'  cardiac  symptoms,  may  be  sufficient  to  upset 


'  I  am  of  course  speaking  of  acute  simple  endocarditis,  not  of  tlie  ulcerative 
variety  of  the  disease. 

-  All  of  these  conditions  are  rare  in  simple  endocarditis.  Ulceration  and  rup- 
ture of  the  valves  are  much  more  common  in  the  infective  than  in  the  simple  form 
of  endocarditis.  Obstruction  of  the  valvular  orifices  by  vegetations  is  of  theoretical 
rather  than  practical  importance,  and  is  more  likely  to  occur  in  the  ulcerative  form. 


Physical  Signs  of  Acute  Endocarditis.  371 

the  balance,  and  to  produce  serious  indications  of  cardiac 
failure  (palpitation,  shortness  of  breath,  congestion  of  the 
lungs,  dropsy,  etc.) 

(c)  The  endocarditis  is  complicated  with  pericarditis 
(endo-pericarditis),  or  with  myocarditis  (endo-myocarditis). 
In  cases  of  this  description,  in  which  cardiac  symptoms  are 
often  very  prominent,  the  clinical  picture  is  of  course  a  com- 
plicated one.  A  severe  attack  of  endo-pericarditis  is  attended 
with  symptoms  similar  to  those  previously  described  (see 
page  31 1);  while  in  endo-myocarditis,  palpitation,  irregular  and 
tumultuous  action  of  the  heart,  a  quick,  weak,  irregular  pulse, 
dyspnoea,  dropsy,  and  other  symptoms  of  cardiac  failure  and 
of  mechanical  interference  with  the  course  of  the  circulation, 
are  apt  to  arise. 

Physical  signs. — The  physical  signs  of  acute  simple  endo- 
carditis are  somewhat  uncertain  ;  and  it  is  in  consequence  of 
this  fact  that  opinions  differ  so  widely  as  to  the  frequency 
with  which  the  condition  occurs  in  acute  rheumatism. 

Inspection,  palpation,  and  percussion  fail,  as  a  rule,  to  give 
any  definite  information,  and  it  is  only  when  the  inflammatory 
changes  are  sufficiently  severe  to  produce  valvular  incom- 
petence,— when,  in  short,  the  normal  heart  sounds  are  replaced 
b\'  murmurs,— that  the  condition  can,  with  any  approach  to 
certainty,  be  recognised. 

We  have  seen  that  the  mitral  valve  is  more  frequenth^  and 
more  severely  attacked  than  the  aortic  ;  we  further  know 
that  incompetence  is  much  more  readily  produced  at  the 
mitral  than  at  the  aortic  orifice ;  hence  it  will  be  easily 
understood  that  a  systolic  murmur  at  the  apex,  which 
indicates  mitral  regurgitation,  is  the  physical  sign  which  is 
most  frequently  met  with  in  these  cases.  It  must,  however, 
be  confessed  that  the  exact  value  of  this  physical  sign  {i.e.  of 
a  systolic  apex  murmur)  as  an  indication  of  acute  endocarditis 
is  by  no  means  settled  ;  and  as  the  question  is  one  of  great 
practical  importance,  I  must  consider  it  in  some  detail.  I 
shall  limit  my  remarks  to  rheumatic  endocarditis,  which 
includes  the  great  majority  of  cases. 


372  Diseases  of  t lie  Heart. 

Most  observers  will,  I  suppose,  agree,  that  in  a  large  pro- 
portion of  cases  of  acute  rheumatism  in  which  the  heart  was 
previously  healthy,  a  systolic  apex  murmur,  in  other  words, 
mitral  regurgitation,  is  developed ;  and  the  great  practical 
question  which  we  have  to  consider  is,  what  is  the  value  of 
that  murmur  as  an  indication  of  acute  endocarditis  ? 

Now  mitral  regurgitation  arising  under  such  circumstances 
ma}-  theoretically  be  due  to  : — 

1.  Organic  changes  in  the  valve  flaps,  the  result  of  endo- 
carditis. 

2.  Relative  or  muscular  incompetence,  the  result  of  rheu- 
matic myocarditis. 

3.  Relative  or  muscular  incompetence,  the  result  of  mus- 
cular debility,  induced  by  the  febrile  process,  independently 
of  rheumatic  myocarditis. 

4.  Relative  or  muscular  incompetence,  the  result  of  anaemia, 
which  is  always  to  a  greater  or  less  extent  developed  in  the 
course  of  a  case  of  acute  rheumatism, — and  which  may  of 
course  be  present  before  the  attack  commenced.^ 

Now  in  trying  to  determine  which  of  these  is  the  true 
cause  of  the  condition,  the  argument,  which  has  been  so 
ably  advanced  by  Dr.  Sansom,  as  to  the  period  of  the 
attack  at  which  the  murmur  is  first  observed  is,  I  think,  of 
the  greatest  importance.'-  He  has  directed  attention  to  the 
fact,  that  in  rheumatic  fever  the  systolic  apex  murmur  is 
generally  developed  early  in  the  attack,  whereas  in  other 
febrile  diseases,  such  as  typhoid,  typhus,  etc.  (in  which  mitral 
regurgitation,  due  to  febrile  changes,  so  to  speak,  in  the 
cardiac  muscle,  is  common,  and  in  which  endocarditis  is  rare), 
the  systolic  apex  murmur  is  developed  late  in  the  attack. 
He,  therefore,  concludes,  and  I  think  with  great  justice,  that 

'  I  am  speaking  of  the  ordinary  rheumatic  fever  of  adults.  In  children,  and 
sometimes  also  in  adults,  acute  rheumatism  is  so  mild  as  not  to  be  attended  by 
anajmia.  Nevertheless  in  these  cases,  more  especially  in  children,  there  is  a 
strong  tendency  to  endocarditis.  This  argument  may  be  added  to  those  which 
will  afterwards  be  advanced  against  the  anemic  origin  of  the  systolic  apex  mur- 
mur which  so  frequently  appears  in  the  course  of  rheumatic  fever. 

*  Ldtsoniiaii  Lectures,  p.  18. 


Physical  Signs  of  Acute  Endocarditis.  373 

the  cause  of  the  mitral  regurgitation,  which  appears  early  in 
acute  rheumatism,  is  not  identical  with  the  cause  of  the  mitral 
regurgitation  which  develops  late  in  typhoid  and  typhus, — 
that  it  cannot  in  short  be  due  to  simple  febrile  changes^  in 
the  cardiac  muscle. 

For  the  same  reason  it  cannot  be  anaemic.  The  murmur 
is  in  fact  developed  before  the  anaemia.  I  am  speaking  of  the 
general  run  of  cases.  An  attack  of  acute  rheumatism  may 
of  course  occur  in  a  person  who  is  anaemic  (in  fact  it  would 
appear  that  anaemia  is  a  predisposing  cause  of  acute  rheu- 
matism), and  in  such  a  case,  the  mitral  murmur  might  be  anaemic, 
and  not  endocarditic.  But  an  apex  systolic  murmur  due  to 
anaemia  would  in  all  probability  be  accompanied  by  a  well- 
marked  basic  (pulmonary)  systolic  murmur.  As  a  matter  of 
fact,  however,  the  mitral  sj^stolic  murmur  which  occurs  in 
the  early  stages  of  acute  rheumatism,  is  not,  as  a  rule,  preceded 
or  accompanied  by  a  pulmonary  systolic  murmur.  Further, 
we  know  that  in  the  later  stages  of  acute  rheumatism,  i.e.  at  the 
period  of  the  attack  when  the  anaemia  does  become  developed, 
pulmonary  systolic  murmurs  are  frequently  observed." 

We  are  obliged,  therefore,  to  conclude  that  the  mitral  re- 
gurgitation, which  accompanies  the  earlier  stages  of  acute 
rheumatism,  must  be  due  to  some  condition  or  conditions 
peculiar  to  the  rheumatic  attack.  We  also  know  that  endo- 
carditis and  myocarditis  do  frequently  occur  in  acute  rheuma- 
tism, that  in  fact  murmurs  of  the  kind  we  are  at  present  consi- 
dering often  become  permanent,  and  are  found  after  death  to 
be  associated  with  organic  mitral  disease. 

It  is  reasonable  to  conclude,  therefore,  that  the  regurgita- 
tion is  due  to  one  or  other  or  both  of  these  conditions  (endo- 
carditis or  myocarditis). 

It  is  much  more  difficult  to  solve  the  second  part  of  the 
problem,  and  to  come  to  a  positive  conclusion  as  to  whether 

•  I  am  of  course  aware  that  M.  Hayem  and  others  consider  the  changes  in  the 
cardiac  muscle,  which  occur  in  typhoid  and  typhus,  inflammatory  in  nature. 
What  I  mean  to  emphasise  is,  that  they  are  not  of  the  same  character  as  the 
rheumatic  changes. 

■^  Sibsoii,  Russell  Rtynolds''  System  of  Medicine,  vol.  iv.  p.  489. 


374  /diseases  of  the  Heart. 

the  regurgitation  is  due  to  organic  changes  in  the  valve  flaps, 
the  result  of  endocarditis,  or  to  'relative'  or  'muscular'  in- 
competence, the  result  of  myocarditis.^ 

It  is,  I  think,  quite  open  to  doubt  whether  the  slight 
organic  chantjes,  which  we  see  in  the  mitral  valve  after  death 
in  some  cases  of  acute  rheumatism  in  which  a  systolic  apex 
murmur  was  present  during  life,  could  have  been  the  cause 
{i.e.  the  mechanical  cause)  of  the  regurgitation.  Inflammation 
of  the  valve  cannot  of  course  produce  regurgitation  except  by 
producing  softening  or  yielding  of  the  flaps,  or  by  leading 
to  the  formation  of  vegetations  sufficiently  extensive  to  pre- 
vent the  perfect  adaptation  of  its  edges.^ 

Further,  recent  observations  go  to  show,  that  in  these  cases 
the  inflammatory  changes  are  not  limited  to  the  parts  of  the 
valves  which  appear  diseased  to  the  naked  eye  ;  but  that  a 
corpuscular  infiltration  extends  all  through  the  endocardium 
and  even  between  the  muscular  fibres  of  the  heart. 

Again,  we  know  that  vegetations  may  be  present  on 
the  mitral  valve  flaps,  and  yet  there  may  have  been  no 
regurgitation,  as  evidenced  by  a  systolic  apex  murmur  during 
life. 

For  all  these  reasons  it  is  difficult  to  exclude  the  influence 
of  the  myocardium.  We  must,  I  think,  allow  that  the 
regurgitation  is  not  in  all  cases  due  to  mechanical  changes 
produced  in  the  valve  flaps  by  inflammation  of  the  endo- 
cardium, but  that  in  some  cases,  if  not  in  all,  the  inflam- 
matory changes  in  the  m)'ocardium  (more  especially  in  the 
mitral  sphincter  and  the  papillary  muscles)  play  an  important 
part  in  its  production. 

But  this  admission  does  not,  in  my  opinion,  detract  from 

'  It  is  probably  impossible  to  give  a  positive  opinion  on  the  point.  What  we 
want  is  a  series  of  post-mortem  examinations,  with  careful  microscopical  observa- 
tion of  the  condition  of  the  valves  and  muscle  in  the  earlier  stages  of  acute 
rheumatism.     It  is  only  by  this  means  that  we  can  hope  to  determine  : — 

(i)  Whether  in  all  cases  in  which  endocarditis  is  present,  there  are  also 
changes  in  the  myocardium. 

(2)  Whether  endocardial  changes  are  present  or  not  in  all  cases  in  which  a 
mitral  murmur  is  observed  in  the  early  stages  of  acute  rheumatism. 

^  Sibsou,  Russell  Re\7iolds'  System  of  Medieine,  vol.  iv.  p.  475. 


Physical  Signs  of  Acute  Endocai'ditis.  375 

the  importance  of  the  murmur  as  a  sign  of  endocarditis.  All 
the  evidence,  which  \vc  at  present  possess,  goes,  I  think,  to 
show  that  endocarditis  very  generally  accompanies,  if  it  does 
not  cause,^  the  inflammatory  changes  in  the  myocardium  to 
which  I  have  just  alluded. 

It  has  also  been  argued  that  since  in  many  of  these 
cases  the  murmur  disappears,  endocarditis  could  not  have 
been  present  ;  for,  it  is  said,  when  a  valve  is  once  attacked 
with  endocarditis  and  rendered  incompetent,  the  valvular 
changes  never  disappear. 

Such  a  conclusion  is,  I  conceive,  untenable. 

In  the  first  place,  it  is  impossible  in  most  cases  to  deter- 
mine by  any  clinical  test  with  which  we  are  acquainted, 
whether  the  regurgitation  will  disappear  or  whether  it  will 
remain  ;  in  other  words,  whether  the  derangement  of  the 
heart  will  or  will  not  terminate  in  organic  disease.  To  decide 
the  question,  as  it  usually  is  decided,  by  the  result,  and  to  say 
that  in  those  cases  in  which  a  valvular  lesion  remains  there 
was  endocarditis,  and  in  those  cases  in  which  no  valvular 
lesion  remains  there  was  no  endocarditis,  is  by  no  means 
satisfactory.  It  would,  in  my  opinion,  be  much  more  logical 
to  conclude  that  the  same  morbid  process  was  present  in  both 
cases ;  that  in  some  cases  the  inflammatory  changes  were 
slight,  and  were  (so  far  as  clinical  examination  can  detect) 
completely  recovered  from  ;  while  in  other  cases  they  were 
more  severe,  and  were  followed  by  structural  changes,  and  the 
usual  physical  signs  of  valvular  disease. 

In  the  second  place,  I  believe,  in  opposition  to  the  gene- 
rally received  opinion,  that  inflammatory  changes  affecting 
the  mitral  valve  often  do  result  in  complete  recovery  so  far 
as  the  functions  of  the  valve  are  concerned  ;  in  other  words, 
that  in  many  cases  of  acute  rheumatism  in  which  an  apex 
systolic  murmur  was  present  during  the  attack,  and  sub- 
sequently disappeared  leaving  the  heart,  so  far  as  clinical 
observations  could  detect,  perfectly  healthy,  the  mitral  valve 

'  The  inflammatory  process,  in  some  cases  at  all  events,  seems  to  spread  from 
the  endocardium  to  the  adjacent  fibrous  tissue  between  the  muscular  fibres. 


376  Diseases  of  the  Heart. 

was  actually  affected  by  endocarditis  during  the   rheumatic 
attack.^ 

I  see  no  reason  why  vahular  changes  sufficient  to  produce 
slight  incompetence  (such,  for  example,  as  corpuscular  infiltra- 
tion of  the  valve  segments  and  adjacent  parts  of  the  myo- 
cardium, and  small  vegetations)  should  not  be  absorbed,  so  as 
to  allow  the  valve  to  become  competent  again.  Indeed  both 
clinical  and  pathological  experience  is,  I  think,  in  favour  of 
such  a  view.  It  must  be  remembered  that  all  degrees  of  en- 
docarditis occur.  After  death  slight  thickenings  of  the  mitral 
valve  are  often  found  in  the  bodies  of  persons  who  have 
previously  suffered  from  acute  rheumatism,  but  who  did  not 
present  any  mitral  murmur  previous  to  death  ;  in  such  cases, 
endocarditis  was,  I  suppose,  present  during  the  rheumatic 
attack,  but  the  valve  had  afterwards  become  completely  com- 
petent. Again,  persons  who  have  recovered  from  acute  rheu- 
matism with,  it  is  said,  healthy  hearts  {i.e.  in  whom  a  mitral 
murmur,  if  it  did  exist  during  the  earlier  stages  of  the  attack 
disappeared  during  convalescence)  are  more  liable  to  be  affected 
with  mitral  valve  disease  in  after  life  than  other  members  of 
the  community  ;  and  one  cause  of  their  greater  liability  to 
subsequent  disease  is  probably  to  be  explained  by  supposing 
that  slight  valvular  changes  (insufficient  to  produce  regurgita- 
tion, and  therefore  unattended  by  a  murmur)  remained  as  the 
result  of  rheumatic  endocarditis,  which  in  after  years  formed 
the  starting  point,  as  it  were,  for  serious  organic  disease. 

The  evidence  which  is  afforded  by  the  examination  of 
cases  of  chorea,  and  which  I  have  stated  below  in  the  form  of 
propositions,  very  strongly  corroborates  the  view  advanced 
above.     It  is  as  follows  : — 

'  I  do  not  say  that  the  mitral  regurgitation  directly  resulted  from  these  valvular 
changes ;  it  may  have  been  due  to  an  associated  affection  of  the  '  mitral  muscle.' 
This  question  has  already  been  discussed.  I  do  however  say,  that  whatever  the 
cause  of  the  regurgitation  (whether  mechanical  changes  in  the  valve  segments  the 
result  of  endocarditis,  or  dynamic  changes  in  the  mitral  sphincter  the  result  of 
myocarditis)  the  strong  probability  is,  that  the  mitral  valve  was  affected  with 
inflammation,  and  that  the  inflammatory  changes  did  not  progress  and  lead  to  a 
permanent  valvular  lesion,  but  that  the  recovery  was  complete,  so  far  as  the  func- 
tions of  the  valve  were  concerned. 


Physical  Signs  of  Acute  Endocarditis.  377 

1.  In  a  large  number  of  cases  of  chorea  a  systolic  mitral 
murmur  is  present. 

2.  In  the  majority  of  these  cases  the  murmur  completely 
disappears,  leaving  the  heart  perfectly  healthy  so  far  as  can 
be  ascertained  by  clinical  tests. 

3.  In  the  vast  majority  of  cases  which  happen  to  prove 
fatal,  either  during  or  shortly  after  an  attack  of  chorea,  a 
fringe  of  bead-like  vegetations  is  found  on  the  mitral  valve. 
This  change  is  found  not  only  in  those  cases  which  die  from 
the  chorea,  and  in  which  there  were  cardiac  symptoms,  but 
in  cases  which  die  from  accidental  or  other  complications,  and 
in  which  there  were  no  cardiac  symptoms  ;  in  cases,  in  short, 
which,  so  far  as  the  heart  symptoms  and  physical  signs  arc 
concerned,  differ  in  no  respect  from  those  which  recover  with- 
out any  cardiac  valvular  disease  remaining. 

4.  In  those  cases  in  which  the  patient  recovers  from  chorea 
and  dies  after  an  interval,  the  valve  is  generally  found  to  be 
perfectly  normal.  '  It  is  only,'  says  Dr  Sturges,  '  where  death 
supervenes  in  the  course  of  chorea  or  very  shortly  after- 
wards, that  this  appearance  is  met  with,  and  in  those  cases 
not  always.'^ 

From  this  evidence  wc  are,  I  think,  warranted  in  con- 
cluding, that  in  cases  of  chorea  which  present  the  physical 
signs  of  mitral  regurgitation,  a  bead-like  fringe  of  vegetations 
is  generally  present  on  the  mitral  valve  during  the  stage  of 
chorea,  and  that  it  subsequently  disappears  {i.e.  is  absorbed). 

Further,  we  may,  I  think,  conclude  that  the  vegetations 
in  chorea  are  indicative  of  endocarditis,  and  that  they  are 
strictly  analagous  to  the  vegetations  which  appear  on  the 
valves  in  rheumatic  endocarditis  ;  in  fact,  in  many  cases  the 
choreic  endocarditis  is  undoubtedly  rheumatic. 

If  then  choreic  endocarditis  with  vegetations  can  be 
completely  recovered  from,  why  cannot  rheumatic  endo- 
carditis with  vegetations  be  recovered  from  ? 

The  disappearance  therefore  of  the  mitral  murmur  does 
not,  in  my  opinion,  prove  that  endocarditis  was  not  present. 
Further,  if  we  grant,  as  is  probably  the  case,  that  the  mitral 

Chorea,  p.  69. 


3/8  Diseases  of  tJie  Heart. 

regurgitation  which  is  present  in  so  many  cases  of  acute 
rheumatism,  is  in.  part  at  least  due  to  the  condition  of 
the  cardiac  muscle  (the  corpuscular  infiltration  of  the  myo- 
cardium) we  can  still  more  easily  understand  how  on  the 
subsidence  of  the  inflammation,  and  the  absorption  of  the 
inflammatory  products,  the  muscular  closure  of  the  valve 
may  again  be  perfectly  effected,  and  the  murmur  may  dis- 
appear.^ 

The  conclusions  therefore  to  which  I  would  come,  with 
regard  to  the  value  of  a  systolic  mitral  murmur  in  acute 
rheumatism  are  as  follows  : — 

1.  That  a  systolic  mitral  murmur  occurring  in  the  early 
stages  of  a  first  attack  of  acute  rheumatism,  in  a  person  free 
from  previous  valvular  disease  and  not  previously  anaemic, 
shows  that  there  is  a  rheumatic  affection  of  the  heart. 

2.  That  the  mitral  regurgitation  in  such  cases  may  be  due 
cither  to  mechanical  alterations  in  the  valve  segments,  result- 
ing from  endocarditis,  or  to  muscular  incompetence,  the  result 
of  a  rheumatic  affection  of  the  muscle  of  the  heart,  or  to  a 
combination  of  the  two  conditions. 

3.  That  although  it  is  impossible  in  many  cases,  to  deter- 
mine which  of  these  conditions  (valvulitis  or  'muscular' 
incompetence)  is  the  exact  cause  of  the  regurgitation  ;  the 
strong  probability  is,  that  the  endocardium  is  affected. 

I  would  therefore  regard  a  murmur  of  this  description  as 
very  strong  evidence  of  acute  endocarditis. 

4.  That  in  exceptional  cases  the  murmur  (in  the  early 
stages)  is  due  to  anaemia.  In  these  cases  there  would  pro- 
bably be  a  history  of  well  marked  anaemia  ;  a  basic  systolic 
(pulmonary)  murmur  would  also  be  present. 

5.  That  a  mitral  systolic  murmur  originating  in  the  later 
stages  of  acute  rheumatism  may  be  due  to  a  rheumatic  in- 
flammation   of    the    heart     (endocarditis    or    myocarditis)  ; 

•  Dr  Sansom  directs  attention  to  the  fact,  that  in  these  cases  the  subsidence 
of  the  murmur  must  not  be  taken  as  proof  of  the  cure  of  the  endocarditis  ;  for  in 
some  of  them,  at  all  events,  the  process  of  absorption  and  cicatrisation  continues  to 
progress,  the  valvular  orifice  becomes  deformed,  and  the  murmur  indicative  of 
established  organic  disease  appears. 


Physical  Signs  of  Acute  Enclocai'ditis.  379 

anfemia  ;  or  simple  muscular  relaxation  such  as  is  met  with 
in  all  fevers. 

But,  further,  it  has  been  shown,  more  particularly  by  the 
late  Dr  Sibson,  and  by  Sir  Wm.  Gull  and  Dr  Sutton,  that 
the  mitral  systolic  murmur  is  in  many  cases  preceded  by 
a  prolonged  first  sound  ;  that  the  mitral  regurgitation  is  in 
fact,  as  we  would  naturally  expect,  not  abruptly  but  gradually 
established  ;  and  that  for  some  time,  it  may  be  for  some  days, 
before  a  murmur  can  be  distinctly  heard,  the  first  sound  at 
the  apex  is  prolonged,  impure  or  murmurish.  These  writers 
are,  therefore,  of  opinion,  and  with  their  opinion  I  entirely 
agree,  that  a  prolonged  or  impure  first  sound  in  the  early 
stages  of  acute  rheumatism  is  highly  suggestive  of  endo- 
carditis. '  Prolongation  of  the  first  sound,'  says  Sibson,  '  is 
the  first  whisper  of  an  approaching  murmur,  the  last  of  a 
departing  one.  .  .  .  We  must  look  then  upon  prolonga- 
tion of  the  first  sound  as  a  sign  of  actual  or  probable  or 
threatened  inflammation  of  the  heart.'^ 

In  addition  to  these  physical  signs,  others  are  sometimes 
present,  which,  more  particularly  in  severe  cases,  make  the 
diagnosis  still  more  certain. 

Endocarditis  affecting  the  aortic  valve  may  produce  aortic 
regurgitation.  In  such  cases  the  valve  flaps  are  generally 
covered  with  extensive  vegetations,  and  are  not  unfrequently 
ulcerated.  A  double  aortic  murmur  is  then  present,  and  is 
proof  positive  of  serious  organic  disease.^ 

Accentuation  of  the  pulmonary  second  sound,  the  evidence 
of  secondary  changes  in  the  right  heart,  such  as  increased 
dulness  on  percussion,  due  to  rapid  dilatation  ;  signs  of 
pulmonary  congestion  or  mechanical  derangement  of  the 
systemic  venous  circulation — when  developed  in  the  course  of 
acute  rheumatism,  and  independently  of  any  complication  in 
the  lungs  capable  of  seriously  obstructing  the  pulmonary 
circulation — are    of   course  the   strongest    possible    evidence 

'  Russell  Reynolds'  System  of  Medicine,  vol.  iv.  p.  493. 

^  A  systolic  aortic  murmur  may  be  due  to  anaemia,  but  a  diastolic  murmur  is 
always  organic. 


380  Diseases  of  tJie  Heart. 

of  extensive  mitral  regurgitation  ;  and  it  would  be  quite  safe 
to  predict  in  any  case  in  which  extensive  mitral  regurgita- 
tion was  suddenly  developed  in  the  course  of  rheumatic  fever, 
that  endocarditis  with  or  without  myocarditis  was  present.^ 

In  addition,  Dr  Sansom  states  that  in  some  cases  he  has 
observed  reduplication  of  one  or  other  of  the  heart  sounds 
as  an  early  sign  of  endocarditis,  and  so  far  as  his  experience 
enables  him  to  judge,  the  endocarditis  in  cases  of  this  descrip- 
tion has  been  followed  by  stenosis  rather  than  by  regurgi- 
tation.- 

CouipUcations. — In  a  large  proportion  of  cases  of  acute 
endocarditis  there  is  probably  some  inflammatory  infiltra- 
tion of  the  myocardium,  more  especially  of  the  fibrous 
septa  between  the  muscular  fibres  immediately  adjacent 
to  the  endocardium.  It  is  only,  however,  in  a  small  number 
that  the  muscular  substance  of  the  heart  is  permanently 
affected. 

Pericarditis  is  a  more  common  complication  than  severe 
myocarditis — for,  according  to  Sibson's  statistics,  every  third 
case  of  rheumatic  endocarditis  is  complicated  with  peri- 
carditis.^ 

Accidental  complications  due  to  emboli,  such  as  Jiemi- 
plegia,  enlargement  of  the  spleen,  etc.,  are  not  uncommon. 

It  would  be  out  of  place  to  describe  here  the  numerous 
diseased  conditions  which  may  be  associated  with  endo- 
carditis, and  which  depend  upon  the  nature  of  the  primary 
condition,  in  the  course  of  which  the  endocarditis  occurs, 
rather  than  upon  the  endocarditis  itself.  The  albuminuria 
and  dropsy,  which  so  frequently  occur  in  association  with 
scarlatinal  endocarditis,  may  be  instanced  as  an  example. 

'  In  other  words,  acute  myocarditis  rarely  if  ever  produces  per  se  extensive 
mitral  regurgitation  in  a  case  of  acute  rheumatism.  Under  such  circumstances 
endocarditis  is,  I  believe,  almost  invariably  present. 

"  Lettsoiiiian  Lectii7-es,  p.   18. 

^  In  a  total  number  of  326  cases  of  acute  rheumatism  observed  by  Sibson, 
endocarditis  was  present  without  pericarditis  in  108  cases,  and  with  pericarditis 
in  54. — Russell  Reynolds,  vol.  iv.  p.  187. 


Clinical  History  of  Acute  Endccarditis.        381 

Onset,  Duratioji,  and  Terminations. 

Onset. — The  onset  of  uncomplicated  endocarditis  is,  as  a 
rule,  insidious  ;  it  is  only  in  a  small  proportion  of  cases  that 
there  are  any  subjective  sensations  which  direct  attention  to 
the  heart. 

Duration. — It  is  difficult  to  give  any  definite  opinion  as 
to  the  duration.  The  physical  signs  are  uncertain,  and, 
fortunately,  our  opportunities  of  determining  the  point  by 
post-mortem  investigation  are  comparatively  rare.  The 
duration  of  the  apex  systolic  murmur,  in  those  cases  in 
which  there  is  good  reason  to  believe  that  the  mitral 
regurgitation  is  associated  with  endocarditis,  is  probably  our 
best  guide,  though  a  very  imperfect  one  ;  for,  on  the  one 
hand,  the  inflammatory  process  must  have  made  consider- 
able headway  before  the  valve  becomes  incompetent,  and  on 
the  other,  the  valve  may  probably  regain  its  competence  some 
time  before  the  acute  changes  have  subsided. 

Terminations. — It  is  probable,  I  think,  that  in  a  con- 
siderable number  of  cases  in  which  the  inflammatory  changes 
are  slight,  the  products  of  inflammation  are  for  the  most 
part,  if  not  entirely,  absorbed,  the  valve  regains  its  compe- 
tence, and  a  practical  cure  is  effected. 

In  many  cases,  if  not  in  all,  some  thickening  of  the  valve 
segments  remains,  and  in  some  cases  these  thickenings  become, 
in  after  life,  the  starting  points  of  chronic  valvular  lesions. 

It  must,  however,  be  admitted  that  in  the  majority  of 
well-marked  cases  the  termination  is  more  unfavourable. 
The  process  of  absorption  and  cicatricial  contraction  in  a 
considerable  proportion  of  cases  produces  such  structural 
alterations,  that  stenosis  or  incompetence  of  the  valvular 
orifice,  or  a  combination  of  the  two  conditions,  results.  In 
many  cases,  in  short,  a  chronic  valvular  lesion  remains. 
These  valvular  lesions  are,  as  we  shall  afterwards  ^  see,  of  all 
degrees  of  severity,  but   even   in   the   mildest    cases  {i.e.   in 

'  The  future  progress  of  these   cases  will  be   considered   under   the  head   of 
chronic  valvular  lesions. 


J 


82  Diseases  of  tJie  Heart, 


those  cases  in  which  there  are  for  a  time,  it  may  be  for  years, 
no  symptoms  of  cardiac  derangement),  the  ultimate  termina- 
tion is  very  generally  unfavourable. 

In  a  minority  of  cases  the  condition  terminates  fatally 
during  the  acute  or  subacute  stages  of  the  disease,  with  all 
the  clinical  symptoms  and  signs  of  an  advanced  valvular 
lesion  (se.e  440). 

Diagnosis. — When  a  murmur  is  heard  over  the  prrecordial 
region  in  a  case  of  acute  rheumatism  or  other  affection,  in  the 
course  of  which  acute  endocarditis  is  apt  to  arise,  we  must  of 
course  endeavour  to  determine  whether  the  murmur  is  actually 
indicative  of  inflammation  of  the  endocardium  or  not. 

The  steps  in  the  diagnosis  are  as  follows : — 

1.  Is  the  murmur  endocardial  or  exocardial  "l 

2.  If  endocardial,  is  it  due  to  endocarditis? 

3.  If  inflammation  of  the  endocardium  is  present,  is  that 
inflammation  of  the  simple  or  ulcerative  form  .' 

Step  No.  I. — Is  ttie  murmur  endocardial  or  exocardial  ? 

There  is  very  seldom  any  difficulty  in  deciding  whether 
the  murmur  is  produced  within  or  without  the  heart.  In 
those  cases  in  which  the  difficulty  does  arise, — and,  according 
to  Dr  Sansom  it  is  chiefly  in  children  that  this  is  likely  to 
occur, — the  question  can  usually  be  determined  by  reference 
to  the  points  of  distinction  which  have  already  been  de- 
tailed.    (See  table  III.  p.  330.) 

Step.  No.  2. — If  the  murmur  is  endocardial,  is  it  due  to 
inflammation  of  the  endocardium  ? 

In  attempting  to  answer  this  question,  we  have  in  the  first 
place  to  determine  whether  the  murmur  is  an  old  one  or  a 
recent  one.  In  those  cases  in  which  the  condition  of  the 
heart,  prior  to  the  attack  for  which  the  patient  comes  under 
observation,  is  unknown,  it  is  sometimes  difficult  or  impossible 
to  determine  this  point.  We  have  to  rely  chiefly  upon  the 
physical  examination  of  the  heart,  aided  to  some  extent  by 


Diagnosis  of  Ami e  Endocarditis.  38 


o 


the  previous  history  of  the  case.  There  is  Httle  difficulty  in 
those  cases  in  which  well-marked  secondary  changes  in  the 
heart,  such  for  instance  as  hypertrophy  of  the  left  ventricle, 
or  hypertrophy  and  dilatation  of  the  right  ventricle,  are 
present.  Accentuation  of  the  pulmonary  second  sound,  with 
a  minor  degree  of  dilatation  of  the  right  heart,  is  also 
suggestive  of  an  old  valvular  lesion  ;  but  the  evidence  is  then 
by  no  means  so  conclusive,  for  acute  dilatation  of  the  heart 
is  sometimes  observed  in  endocarditis  (rarely  however  in  the 
early  stages  of  the  condition)  ;  and  mitral  regurgitation, 
sufficiently  free  to  be  attended  with  considerable  increase  of 
the  blood-pressure  within  the  pulmonary  artery,  and,  there- 
fore, with  well-marked  accentuation  of  the  pulmonary  second 
sound,  is  of  frequent  occurrence  during  the  acute  stage  of 
endocardial  inflammation. 

A  history  of  shortness  of  breath  on  exertion,  of  swelling  of 
the  feet,  or  of  other  well-marked  cardiac  symptoms,  is  very 
strong  evidence  of  old  disease. 

The  occurrence  of  a  previous  attack  or  attacks  of  acute 
rheumatism  is  also  suggestive  of  old  organic  disease. 

It  must,  however,  be  remembered  that  old  valvular  disease 
does  not  exclude  recent  endocarditis,  on  the  contrary,  it 
rather  favours  its  development.  In  all  cases  of  acute 
rheumatism,  in  which  we  are  satisfied  of  the  existence 
of  an  old  valvular  lesion,  we  should  strongly  suspect  the 
presence  of  recent  inflammation  ;  and  in  cases  of  this 
description,  in  which  the  cardiac  symptoms  undergo  notable 
and  sudden  aggravation  during  the  rheumatic  attack,  the 
presence  of  acute  endocarditis  is  almost  certainly  indicated. 
In  those  cases  in  which  the  murmur  is  a  recent  one  (/>. 
has  developed  during  the  present  attack),  and  in  which 
the  symptoms  and  signs  of  valvular  lesion  are  rapidly 
developed,  there  is  of  course  no  difficulty.  The  occurrence 
of  a  presystolic  mitral  or  tricuspid,  or  of  a  diastolic  aortic 
or  pulmonary  murmur,  under  such  circumstances,  is  quite 
conclusive,  whether  the  murmur  is  attended  with  cardiac 
symptoms  or  not,  for  these  murmurs  always  depend  upon 
mechanical  changes  in  the  valve  flaps  or  valvular  orifices. 


384  Diseases  of  the  Heaii. 

There  is  much  more  difficulty  when,  as  is  usually  the  case, 
the  murmur  is  systolic.  I  have  already  detailed  in  full  the 
reasons  which  lead  me  to  regard  a  mitral  systolic  murmur 
or  impure  first  sound,  occurring  in  the  early  stages  of  an 
attack  of  acute  rheumatism,  and  in  a  person  previously  free 
from  cardiac  disease  or  marked  anaemia,  as  highly  suggestive 
of  acute  endocarditis. 

The  same  murmur  (a  mitral  systolic  murmur)  when  it 
occurs  in  the  later  stages  of  the  attack,  is  possibly  anaemic  in 
character,  more  especially  if  the  patient  is  markedly  anaemic, 
and  if  the  development  of  the  mitral  murmur  is  preceded  by 
a  pulmonary  sj-stolic  murmur  ;  but  it  is  impossible  to  give 
a  positive  opinion  on  the  point.  The  murmur  may  be 
organic  ;  and  the  wise  physician,  while  hoping  for  the  best 
[i.e.  that  it  is  anaemic),  will  take  every  precaution,  and  treat 
the  patient  as  if  the  murmur  depended  upon  organic  disease. 

A  basic  s)'stolic  murmur,  aortic  or  pulmonary  (but 
especially  the  latter),  which  develops  late  in  the  attack,  and 
when  the  patient  is  anaemic,  is  very  generally  functional. 

Murmurs  which  are  loud  and  well  propagated  are 
generally  organic,  musical  murmurs  are  always  so. 

Step  No.  J. — //  inf  animation  of  the  endocardium  is  present, 
is  that  inflammation  of  the  simple  or  ulcerative  form  ? 

The  consideration  of  this  question  must  be  deferred  until 
the  ulcerative  form  of  endocarditis  has  been  described.  (See 
page  41 1.) 

Prognosis. — In  forming  the  prognosis  the  following  points 
must  be  taken  into  account : — 

(i)  The  nature  and  severity  of  the  primary  affection  with 
which  the  endocardial  inflammation  is  associated. 

(2)  The  state  of  the  heart  itself 

(3)  The  condition  of  the  other  tissues  and  organs. 

In  rheumatic  endocarditis,  the  immediate  result  is  usually 
favourable,  but  some  cases  die,  as  we  have  seen,  during  the 
acute  or  subacute  stages  of  the  disease. 

Symptoms  indicative  of  grave  mechanical  derangement  of 


Proojwsis  of  Aaite  Endccarditis.  385 

the  circulation,  and  of  failure  of  the  heart,  such  as  dyspnoea, 
dropsy,  cyanosis,  a  quick,  weak,  and  irregular  pulse,  are  very 
serious  indications.  Cases  in  which  aortic  regurgitation  is 
acutely  established  are,  as  a  rule,  more  serious  than  those  in 
which  the  mitral  valve  is  affected. 

Pericarditis,  and  more  particularly  myocarditis,  add  to  the 
gravity  of  the  attack.  The  existence  of  previous  valvular  dis- 
ease, other  things  being  equal,  materially  increases  the  danger. 

The  ultimate  prognosis  is  in  a  large  proportion  of  cases 
unfavourable,  for  many  patients,  who  recover  from  the  acute 
affection,  ultimately  suffer  and  die  from  chronic  valvular 
disease.  The  prognosis  should  always,  therefore — even  in  the 
mildest  cases — be  guarded,  for  so  long  as  the  slightest  indica- 
tions of  endocarditis  are  present,  it  is  impossible  to  be  certain 
that  serious  valvular  lesions  may  not  remain.  The  disappear- 
ance of  the  systolic  apex  murmur,  which  is  the  most  common 
physical  sign  of  endocarditis,  is,  of  course,  the  most  favourable 
indication.  It  is  not,  however,  proof  positive  of  the  cure  of 
the  endocarditis,  for,  as  Dr  Sansom  has  shown,  the  regurgita- 
tion may  have  been  due  to  an  affection  of  the  myocardium 
rather  than  of  the  endocardium  ;  the  corpuscular  infiltration 
of  the  myocardium  may  be  absorbed  ;  the  valve  may  become 
competent ;  but  the  endocardial  cicatrix,  so  to  speak,  may 
continue  to  contract,  and  a  murmur  indicative  of  organic 
valve  disease  may  in  a  short  time  be  established.  In  all 
cases,  therefore,  the  heart  should  be  examined  from  time  to 
time  during  the  period  of  convalescence.  The  character  of 
the  murmur  and  the  condition  of  the  heart  must,  of  course, 
be  taken  into  consideration.  A  soft  valvular  murmur,  which 
is  not  well  propagated,  and  which  is  not  attended  by  any 
marked  accentuation  of  the  pulmonary  second  sound  or  by 
secondary  changes  in  the  right  heart,  very  often  disappears 
without  leaving  any  organic  change  behind.  Vice  versa  the 
lesion  is  a  serious  one  in  those  cases  in  which  the  murmur  is 
heard  below  the  angle  of  the  left  scapula,  in  which  the  second 
sound  is  accentuated,  and  more  especially  in  which  there  are 
secondary  changes  in  the  right  heart  (increased  dulness  result- 
ing from  dilatation,  a  systolic  tricuspid  murmur,  etc.). 

BB 


J 


86  Bisrasc's  of  tJic  Heart. 


A  murmur,  which  continues  after  convalescence  is  fully 
established,  may,  in  exceptional  cases,  disappear  at  the  end  of 
some  months.  As  a  rule,  however,  such  a  murmur,  and  the 
organic  changes  on  which  it  depends,  are  permanent.  The 
extent  and  severity  of  the  lesion  which  remains,  vary  greatly 
in  different  cases.  Each  case  must  of  course  be  judged 
on  its  own  merits  in  accordance  with  the  principles  which 
will  be  described  when  I  come  to  treat  of  chronic  valvular 
lesions. 

Treatment. — As  in  the  case  of  pericarditis,  it  is  necessary 
to  consider  both  the  prophylactic  and  curative  treatment  of 
the  affection. 

Prophylactic  treatment. — Since  acute  simple  endocarditis 
is  seldom  primary,  but  usually  occurs  in  the  course  of  some 
other  disease,  our  prophylactic  measures  must  be  directed  : — 

(i)  To  ivarding  off  or  preventing  the  primary  affection  zuith 
ivhich  it  is  apt  to  he  associated. 

Space  does  not  allow  me  to  enter  into  details  as  to  the 
manner  in  which  acute  rheumatism,  chorea,  scarlet  fever, 
measles,  diphtheria,  pyaemia,  puerperal  fever,  and  the  other 
affections  with  which  endocarditis  is  apt  to  be  associated,  are 
to  be  prevented.  The  prophylactic  of  these  affections  consists, 
of  course,  in  avoiding  the  causes — both  predisposing  and 
exciting — which  produce  them.  The  reader  who  wishes 
further  information  on  this  subject  must  consult  some  of  the 
standard  works  in  which  the  aetiology  of  these  affections  is 
fully  treated  of. 

(2)  To  aire  the  primary  affection,  luhen  once  it  is  established, 
as  speedily  as  possible,  and  in  particular  to  adopt  sncJi  a  plan  of 
treatment  as  is  most  likely  to  prevent  inflammation  of  the  endo- 
cardium. 

Applying  this  indication  to  the  treatment  of  acute  rheu- 
matism, which  is,  as  we  have  repeatedly  seen,  by  far  the  most 
common  cause  of  acute  endocarditis,  we  must  endeavour  to 
cut  short  the  rheumatic  attack,  to  allay  the  pain  and  fever  as 
speedily  as  possible,  and  to  enforce  a  rigid  system  of  rest,  for, 
as  Sibson  has  shown,  the  relief  of  pain  and  suffering,  together 


Treatment  of  Acute  Endocarditis.  387 

with  absolute  rest,  exerts  a  most  beneficial  influence  in  pre- 
venting cardiac  complications. 

Sibson's  observations  on  this  point  are,  I  think,  of  extreme  importance, 
and  have  a  very  direct  bearing  upon  the  treatment  of  acute  rheumatism 
bysahcin  and  its  compounds.  I  make  no  apology,  therefore,  for  quoting 
what  he  says  in  full.  He  states  : — 'We  here  find  that  in  the  series  of 
cases  of  acute  rheumatism  that  were  treated  by  a  system  of  absolute  rest, 
the  proportion  of  those  that  were  attacked  with  endocarditis  was  slightly 
less  than  that  of  those  that  were  not  so  treated.  Thus  far  the  comparison 
is  but  slightly  in  favour  of  the  treatment  of  acute  rheumatism  by  a  rigid 
system  of  rest  ;  and  this  would  seem  to  suggest  that  a  certain  and  a  very 
large  proportion  of  cases  of  acute  rheumatism  are  habitually  and  in- 
trinsically attacked  by  endocarditis.  When,  however,  we  extend  the 
comparison,  and  ascertain  the  proportion  in  which  those  cases  of  endo- 
carditis, not  previously  so  affected,  acquired  permanent  valvular  disease, 
so  as  to  injure  health  during  the  remainder  of  life,  and  to  shorten  life 
itself,  we  discover  that  the  series  of  cases  not  treated  by  a  system  of 
absolute  rest  were  thus  permanently  injured  in  a  far  larger  proportion  of 
cases,  amounting  to  more  than  twice  as  many,  or  in  the  ratio  of  eight  to 
three,  than  in  those  that  were  treated  by  rest. 

'If  we  pursue  the  inquiry  further,  so  as  to  discover  the  relative  extent 
to  which  the  interior  of  the  heart  was  inflamed  in  the  two  series  of  cases, 
we  discover  that  there  was  but  one  instance,  or  i  in  24,  of  those  with  endo- 
carditis and  without  previous  valvular  disease,  of  the  series  treated  by  a 
rigid  system  of  rest,  that  gave  definite  evidence  of  inflammation  of  both 
the  aortic  and  mitral  valves,  while  in  19  instances  in  127,  or  i  in  67 
of  the  same  kind  of  cases  that  were  not  treated  by  a  rigid  system  of  rest, 
there  was  direct  evidence  of  aortic  regurgitation.  In  nine,  or  rather  ten, 
of  those  cases  that  were  not  treated  by  rest,  there  was  a  mitral  murmur, 
and  therefore  direct  evidence  of  inflammation  of  the  mitral  vahe  ;  but  in 
the  remaining  nine  cases  there  was  also  evidence  of  mitral  endocarditis 
in  the  shape  of  a  tricuspid  murmur,  or  prolongation  of  the  first  sound, 
with  intensification  of  the  pulmonic  second  sound,  and  obstacles  to  the 
flow  of  blood  through  the  lungs.^     The  whole  chain  of  e\idence  points 

'  There  will  probably  be  considerable  difference  of  opinion  as  to  the  exact  value 
which  these  physical  signs  possess  as  evidence  of  acute  endocarditis.  In  the 
absence  of  any  obstruction  in  the  lungs,  they  are  indicative  of  some  embarrassment 
in  the  left  heart.  Now,  considering  the  frequency  of  acute  endocarditis  in  acute 
rheumatism,  and  the  frequency  with  which  a  systolic  mitral  murmur  and 
permanent  evidence  of  valve  disease  spring,  as  it  were,  directly  out  of  these 
physical  signs,  I  am  personally  disposed  to  think  that  when  they  are  met  with  in 
the  early  stage  of  the  attack,  and  are  unassociated  with  anaemia  and  basic  cardiac 
murmurs,  that  they  are  suggestive  of  endocarditis,  but  certainly  not  a  distinct 
proof  of  its  presence. 


388  Diseases  of  the  Heart. 

then,  I  think,  irresistibly  to  the  conclusion  that  the  extent,  severity,  and 
permanent  ill  effects  of  the  endocarditis  were  much  greater  in  the 
series  of  cases  that  were  not  rigidly  treated  by  rest  than  in  the  series 
that  were  so  treated." 

Now  for  the  relief  of  the  joint  affection  and  the  reduction 
of  the  temperature,  there  is,  I  suppose,  a  concensus  of  opinion, 
that  the  sahcyHc  treatment  is  better  than  any  other.  Twenty 
to  thirty  grains  of  saHcin  or  salicylate  of  soda  given  every  two 
hours,  succeed,  in  a  large  proportion  of  cases,  in  completely 
removing  the  joint  affection,  and  in  reducing  the  temperature 
within  forty-eight  hours.  If  then  Sibson's  observations  and 
deductions  are  correct,  this  drug  ought  to  exert  a  very 
beneficial  influence  in  preventing  cardiac  complications.  If  it 
does  not  exert  such  a  beneficial  influence,  we  must,  I  think, 
conclude  that,  while  relieving  the  joint  affection  and  fever,  it 
actually  exerts  a  prejudicial  effect  on  the  heart,  rendering  the 
endocardium  more  liable  to  be  affected,  and  neutralising  the 
protective  influence  which  the  relief  of  the  joint  affection  and 
fever  ought,  according  to  Sibson's  observations,  to  produce. 

The  most  extensive  observations  which  have  as  yet  been 
published  on  this  point,  are  those  which  were  brought  forward 
at  the  great  debate  before  the  Medical  Society  of  London  in 
the  year  1881  ;  and  it  seems  to  have  been  pretty  generally 
concluded,  that  the  result  of  the  statistics  then  brought 
forward  was  to  show  that  salicin  and  its  compounds  do  not 
exert  the  protective  influence  in  warding  off  cardiac  complica- 
tions which  we  would  a  priori  have  expected. 

Personally  I  have  considerable  hesitation  in  accepting  that 
conclusion  as  correct,  more  particularly  as  some  of  the  leading 
speakers  in  that  debate  (Drs  Hilton  Fagge,  Broadbent, 
Douglas  Powell,  Havilland  Hill,  and  Herman),  seemed,  on  the 
whole,  to  think  that  the  influence  of  the  salicylic  compounds 
in  preventing  endocarditis  was  favourable,  and  also  for  the 
following  reasons  : — - 

'  Russell  Reynolds'  System  of  Medicine,  vol.  iv.  p.  527. 

*  I  state  these  reasons  with  great  diffidence,  for  I  am  fully  aware  that  it  is  often 
extremely  difficult  to  form  correct  conclusions  upon  figures  and  facts  with  which 
one  is  not  personally  familiar.  Those  who  were  present  at  the  debate,  and  more 
particularly  the  speakers  who  were  familiar  with  all  the  facts  (for  in  analysing 


Trcatiiicut  of  Acute  Endocarditis.  389 

In  the  fij'st  place,  the  result  of  that  debate  was  almost 
entirely  based  upon  hospital  cases  ;  and,  as  Dr  Douglas 
Powell  very  justly,  I  think,  observed,  and  as  Dr  Maclagan^ 
has  pointed  out,  it  is  almost  impossible  to  determine  this 
question  by  the  results  of  hospital  practice.  In  a  large 
proportion  of  hospital  patients,  endocarditis — as  evidenced 
by  a  systolic  apex  murmur — is  already  developed  on  the 
patient's  admission.  These  cases  must,  of  course,  be  ex- 
cluded in  any  inquiry  as  to  the  influence  which  salicin  has 
in  preventing  endocarditis.  Again,  there  is  good  reason  for 
supposing,  as  I  have  previously  pointed  out  in  detail  (see 
p.  379),  that  endocarditis  is  present  at  the  time  of  the  patient's 
admission,  in  many  cases  in  which  there  is  no  murmur,  but  in 
which  a  bruit  subsequently  becomes  audible.  These  cases 
must  also  be  excluded,  for,  as  Dr  Maclagan  puts  it,  '  this 
saving  action  (of  the  salicyl  compounds)  cannot  be  got  unless 
they  are  given  in  adequate  quantity  before  the  poison  has  begun 
to  act  on  the  hearti^  It  may,  of  course,  be  said,  and  the 
argument  doubtless  has  some  force,  that  the  salicyl  com- 
pounds should  not  only  prevent,  but  that  they  should  also 
allay  the  endocardial  inflammation  even  after  it  is  developed. 
There  are  not  the  same  fallacies  in  deciding  this  point,  and 
there  seems  to  be  a  very  general  opinion  that  these  drugs 
have  no  influence  in  this  direction.  Dr  Fagge  'fully  admits 
that  salicylic  acid  seems  to  have  no  power  of  controlling  or 
arresting  the  cardiac  complications  of  acute  rheumatism  when 
once  they  have  developed  themselves.'^ 

Dr  Maclagan  believes  that  when  endocardial  complica- 
tions occur,  '  the  treatment  by  salicylate  of  soda  occasionally 
increases  the  patient's  danger.  I  refer  especially,'  he  says, 
'  to  those  cases  more  numerous  than  is  usually  supposed,  in 
which  the  muscular  substance  of  the  heart  is  the  seat  of  in- 
flammation.    Myocarditis  has,  for  its  pathological  condition, 

such  a  large  number  of  cases  as  were  analysed  by  some  of  the  speakers  in  this 
debate,  it  is  of  course  impossible  to  go  into  every  detail),  were,  of  course,  much 
more  likely  to  come  to  a  more  correct  conclusion  than  I  can  possibly  do. 

'   Rheitviatisia,  p.  271.  ■  Locks  cit.  p.  269. 

^  La7icet,  Dec.  17,  1881,  p.  1033. 


390  Diseases  of  the  Heart. 

thickening-,  softening  and  enfeeblement  of  the  n:mscular  walls, 
chiefly  those  of  the  left  ventricle.  If  to  this  enfeeblement  is 
added  that  which  sometimes  follows  the  administration  of 
salicylate  of  soda,  the  patient's  condition  is  thereby  rendered 
more  serious,  and  the  continuous  administration  of  the 
salicylate  might  turn  the  scale  against  him.'^  It  must  be 
particularly  noted  that  Dr  Maclagan  does  not  believe  that 
salicin  has  this  depressing  influence  on  the  heart.  Dr  Broad- 
bent  is  so  strongly  of  opinion  that  salicyl  and  its  compounds 
are  useless  in  the  cure  of  endocarditis,  that  the  moment  he 
recognises  any  cardiac  inflammation  he  discontinues  their 
administration.- 

In  the  second  place,  all  endocardial  murmurs  are  not 
indicative  of  endocarditis,  in  the  later  stages  of  acute  rheu- 
matism more  especially,  when  anaemic  murmurs  are  most  apt 
to  arise,  there  may  be  great  difficulty  in  deciding  whether 
endocarditis  is  present  or  not. 

In  the  tJiird  place,  observers  are  by  no  means  agreed  as  to 
the  value  which  is  to  be  attached  to  different  endocardial 
murmurs  as  signs  of  endocarditis.  It  is  difficult,  therefore,  to 
compare  the  results  of  different  physicians  who  may  attach 
very  different  values  to  the  same  facts.  It  is  still  more 
difficult  to  compare  the  observations  made  to-day  with  the 
obser\'ations  made  twenty  or  thirty  years  ago. 

Although  personally  I  am  inclined  to  attach  very  great 
importance  to  apex  systolic  murmurs,  arising  in  the  early 
stages  of  acute  rheumatism  and  zvitliont  basic  systolic  (pul- 
monary) murmurs,  as  indicative  of  acute  endocarditis,  I  think 
it  would  be  wise  to  base  our  inquiry  upon  the  number  of  cases 
in  which  permanent  valvular  lesions — as  to  the  symptoms  and 
signs  of  which  there  is  very  general  agreement — remain, 
rather  than  upon  the  frequency  with  which  endocarditis 
occurs  during  the  attack.  The  nature  of  the  valve  lesion 
which  remains  is  also  a  point  of  some  importance,  for,  as 
Sibson  has  shown,  aortic  regurgitation  requires  for  its  produc- 
tion (as  a  general  rule)  a  greater  degree  of  endocardial 
inflammation  than  mitral  lesions. 

'  Lancet,  Jan.  14,  1882,  p.  59.  '  Laucet,  Jan.  28,  1882,  p.  158. 


Treatment  of  Acute  Endocarditis.  391 

There  is  another  reason  why  endocarditis — as  evidenced  by 
an  apex  systohc  murmur — should  not  be  taken  as  the  standard 
in  estimating  the  value  of  the  salicyl  compounds  in  preventing 
rheumatic  endocarditis ;  for  if,  as  most  observers  admit,  these 
drugs  (salicin  according  to  Dr  Maclagan  excepted)  exert  a 
special  depressing  influence  upon  the  heart,  their  use  is  very 
likely  to  be  attended  with  such  relaxation  of  the  cardiac  muscle 
as  will  produce  mitral  regurgitation  (from  muscular  or  relative 
incompetence)  independently  of  endocarditis. 

For  these  reasons  it  is,  I  think,  difficult  to  decide  the 
question  by  means  of  hospital  statistics  ;  and  more  especially 
to  estimate  the  results  by  the  frequency  with  W'hich  endo- 
carditis is  supposed  to  occur  during  the  attack  of  rheumatic 
fever.  The  inquiry  should,  I  think,  be  based  upon  the 
number  of  cases  in  which  permanent  valvular  lesions  remain. 
Cases  in  which  cardiac  lesions  were  known  or  suspected  to 
have  existed  previously,  or  cases  in  which  the  patient  had 
previously  suffered  from  rheumatic  fever,  should  be  rigidly 
excluded.  The  exact  nature  of  the  resulting  valvular  lesion 
should  be  stated.  Instead  of  comparing  hospital  cases  in 
which,  as  we  have  seen,  endocarditis  is  so  often  established 
before  the  patient  comes  under  observation,  the  inquiry 
should  be  based  on  the  results  of  private  practice,  those  cases 
only  being  selected  in  which  the  patient  comes  under 
observation  at  the  very  commencement,  say  within  the 
first  twenty-four  hours  of  the  attack.^ 

To  be  absolutely  accurate,  the  result  would  have  to  be 
based  upon  a  very  large  number  of  cases,  all  observed  by  one 
thoroughly  competent,  reliable,  and  unprejudiced  observer. 
But  since  it  is  impossible  for  any  single  observer  to  meet  with 

'  Cases  which  come  under  the  care  of  the  practitioner  within  twenty-four  hours 
of  the  development  of  the  attack  would,  as  Dr  Hilton  Fagge  pointed  out  in 
introducing  the  discussion  on  the  salicylates  before  the  Medical  Society  of  London, 
be  '  of  far  more  than  the  average  severity,  since  persons  affected  with  the  milder 
forms  of  the  disease  would  often  wait  for  a  time  before  seeking  medical  advice.' 
That  no  doubt  in  some  respects  is  an  objection  ;  but  the  advantages  of  such  a 
method  of  inquiry  are,  I  think,  so  far  as  our  present  purpose  is  concerned,  so 
much  greater  than  those  which  any  other  method  is  likely  to  afford,  that  I  do  not 
hesitate  to  recommend  it  strongly  to  the  profession. 


392  Diseases  of  t lie  Heart. 

an}'thing  like  a  sufficient  number  of  cases  to  serve  as  an 
adequate  basis  of  results,  the  inquiry  would  of  course  have  to 
be  entrusted  to  a  number  of  observers  of  known  accuracy,  and 
it  would  be  of  the  utmost  importance  that  they  should  all 
make  their  observations  on  exactly  the  same  plan. 

In  the  present  position  of  therapeutics  we  would  hardly, 
I  think,  be  warranted  in  making  a  series  of  investigations  with 
the  view  of  testing  the  efficiency  of  different  drugs,  for  I 
thoroughly  agree  with  Dr  Hilton  Fagge  in  thinking,  that  we 
would  not  be  justified  in  withholding  salicin  and  its  com- 
pounds from  our  patients  at  the  commencement  of  rheumatic 
fever  unless  there  were  some  special  contra-indication  to  the 
use  of  the  drug.  But  we  might,  I  think,  determine  much  more 
satisfactorily  by  this  means  than  by  any  other,  the  proportion 
of  cases  in  which  permanent  valvular  lesions  follow  the  sali- 
cylic plan  of  treatment ;  and  this,  I  believe,  is  the  most 
important  point  which  we  wish  to  decide  with  regard  to  the 
treatment  of  acute  rheumatism.  Having  determined  the 
point  in  the  case  of  the  salicylates,  we  would  have  a  fixed 
standard  with  which  to  compare  any  other  method  of  treat- 
ment which  may  in  the  future  lay  claim  to  be  superior  to 
that  which  at  present  we  believe  to  be  the  best. 

The  method  of  case-taking  recommended  by  the  Col- 
lective Committee  of  the  British  Medical  Association,  should 
be  used,  with  the  following  slight  additions  necessary  for  the 
special  purpose  in  hand  : — 

Method  of  case-taking  in  acute  rheumatism,  with  the  object  of 
determining  the  frequency  7vith  -which  perma7ieni  ca^-diac  valvular  lesions 
folloiu  the  salicylic  plan  of  treatment. 

Note  A.  Only  those  cases  of  acute  articular  rheumatism  are  to  be 
recorded  in  which  : 

(i)  The  patient  was  previously  free  from  cardiac  valvular  disease. 

(2)  The  attack  of  rheumatic  fever  is  a  first  attack. 

(3)  The  treatment  is  put  into  force  within  twenty-four  hours  after  the 
first  manifestation  of  symptoms,  i.e.  of  joint  pain. 

B.  In  all  cases  salicin  to  be  used  and  not  salicylate  of  soda  ;  and 
the  drug  to  be  given  after  the  manner  laid  down  by  Dr  Maclagan,  viz.  : 
'  at  least  thirty  grains  every  hour  till  there  is  decided  evidence  of  action, 
and  then  the  dose  should  be  diminished  slowly.'i 

'  RheuniatisJH,  p.  272. 


T^'-eatment  of  Aciite  Endocm-ditis.  393 

C.  Whenever  any  of  these  directions  are  departed  from,  the  exact 
nature  of  the  modification  introduced  must  be  specified  on  the  card. 

D.  \xi  addition  to  the  points  specified  by  the  Collective  Investigation 
Committee  of  the  British  Medical  Association,  the  following  particulars 
must  be  added  : — 

Condition  of  the  heart  (i)  at  the  end  of  convalescence  ;  and  (2)  six 
months  subsequently,  as  regards  : — 

(a)  Position  of  apex  beat. 

(b)  Force  of  impulse. 

(c)  Murmurs  (their  rhythm,  points  of  differential  maximum  intensity, 
direction  of  propagation,  and  sound  characters). 

(d)  Condition  of  pulmonary  second  sound — normal  — increased. 

(e)  Subjective  cardiac  sensations. 

(f)  Signs  of  mechanical  derangement  of  the  circulation. 

In  the  treatment  then  of  acute  rheumatic  endocarditis,  I 
would  strongly  advise  the  administration  of  full  doses  of  pure 
salicin  after  the  manner  recommended  by  Dr  Maclagan,  and 
I  cannot  help  thinking  that  if  this  treatment  were  vigorously 
carried  out  in  the  earlier  stages  of  the  attack,  the  frequency 
of  endocarditis  and  other  cardiac  complications  would  be 
materially  diminished. 

Some  authorities  recommend  that  full  doses  of  alkali 
(thirty  grain  doses  of  bicarbonate  of  potash  every  two  or 
three  hours  until  the  urine  is  alkaline)  should  be  combined 
with  the  salicin,  and  they  adduce  in  support  of  this  plan 
of  treatment  the  highly  favourable  results,  as  regards  the 
cardiac  affection,  obtained  by  Drs  Fuller,  Dickenson  and 
others.  Some  again,  in  addition  to  the  salicin,  advise 
the  local  application  of  blisters  to  the  joints,  as  recom- 
mended by  Dr  Davies.  Personally  I  am  in  the  habit  of 
wrapping  the  affected  joints  in  cotton  wool,  or  cotton  wool 
sprinkled  with  belladonna  and  chloroform  liniment,  as 
recommended  by  Sibson.  When  the  pain  is  very  severe  a 
hypodermic  injection  of  morphia  should  be  administered,  and 
repeated,  if  required,  for  some  hours  must  necessarily  elapse 
before  the  beneficial  effects  of  the  salicin  become  apparent. 
A  rigid  system  of  rest  must  at  the  same  time  be  strictly 
enforced,  the  greatest  care  being  taken  to  avoid  an)-thing, 
such  as  mental  anxiety,  worry,  or  agitation,  which  is  likely  to 
excite  the  action  of  the  heart.     The  patient  must  of  course  be 


394  Diseases  of  the  Heart. 

placed  in  blankets.  During  the  acute  stage,  the  diet  must  be 
entirely  liquid,  and  should  consist  chiefly  of  milk.  The  con- 
dition of  the  bowels  must  also  be  attended  to.  I  do  not,  as 
a  rule,  prescribe  a  purge  quite  at  the  commencement  of  the 
attack  ;  it  is  better,  I  think,  to  wait  a  day  or  two  until  the 
acutencss  of  the  joint  affection  has  subsided.  The  patient 
should  not  be  allowed  to  leave  his  room  for  the  purpose  of 
evacuating  the  bowels,  it  being  of  the  greatest  importance  to 
avoid  exposure  to  cold. 

If  the  salicin  fails  after  a  fair  trial  (four  or  five  days),  I 
would  advise  the  administration  of  quinine  in  combination 
with  alkalis.  However  mild  the  attack,  or  however  rapid  the 
return  to  health,  the  patient  should  be  kept  in  bed  for  at  least 
a  week  after  the  joint  affection  and  the  pyrexia  have 
completely  subsided. 

During  convalescence  all  sources  of  cardiac  excitement, 
both  bodily  and  mental,  must  be  carefully  avoided.  Tonics, 
more  particularly  quinine,  iron  and  arsenic,  should  be  pre- 
scribed. The  greatest  care  must  be  taken  to  avoid  exposure, 
or  anything  which  is  likely  to  bring  on  a  relapse. 

These  are  the  chief  measures  which  I  would  recommend 
in  a  case  of  acute  rheumatism  uncomplicated  by  the  symptoms 
or  signs  of  acute  endocarditis.  But  before  leaving  the  pro- 
phylactic treatment  of  rheumatic  endocarditis,  I  must  again 
direct  attention  to  the  fact  which  Sansom,  Barlow,  and  others 
have  so  justly  emphasised,  that  endocarditis  not  unfrequently 
arises  in  the  course  of  mild  rheumatic  attacks,  and  that  in 
children  more  especially,  in  whom  the  tendency  to  inflam- 
mation of  the  endocardium  is  so  much  stronger  than  it 
is  in  adults,  the  most  trivial  rheumatic  manifestations 
should  always  be  carefully  attended  to.  I  cannot  too 
strongly  endorse  Dr  Sansom's  teaching  on  this  most  import- 
ant point. 

The  propJiyladic  treatment  of  choreic  endocarditis. — There 
are,  as  I  have  previously  pointed  out,  ample  grounds  for 
believing  that  endocarditis  is  of  frequent  occurrence  in  chorea. 
Now,  in  dealing  with  cases  of  chorea,  it   is   of  the   greatest 


Treatment  of  Acute  Endocarditis.  395 

importance  to  keep  this  fact  in  view ;  for  although,  as  a  rule, 
the  endocardial  inflammation  completely  subsides,  leaving  the 
heart  free  from  organic  change  (so  far  as  our  means  of  clinical 
investigation  can  detect,  and  as  the  future  progress  of  the 
case  amply  proves),  in  some  cases  valvular  lesions  are  (either 
immediately  or  in  future  life)  established.^ 

The  same  general  rules  as  to  avoiding  all  cardiac  strain 
and  excitement,  exposure  to  cold,  and  other  conditions  likely 
to  act  as  exciting  causes  of  endocarditis,  and  which  have  been 
already  mentioned  in  speaking  of  the  prophylaxis  of  rheumatic 
endocarditis,  are  equally  applicable  here  ;  and  it  is  the  more 
necessary  to  insist  upon  this  point,  since  chorea  is  too 
generally  regarded  as  a  trivial  affection.  The  patient  should 
be  kept  in  bed  during  the  attack.  Arsenic,  chloral,  and 
bromide  of  potassium,  are  the  remedies  which  I  have  found 
most  useful.  The  bowels  must  be  carefully  attended  to  ;  but 
I  must  refer  the  reader  for  details  of  the  treatment  of  chorea 
to  works  on  general  medicine. 

The  prophylaxis  of  endocarditis  in  scarlet  fever,  measles, 
diphtheria,  pnej'peral  fever,  pyceniia,  etc.  —  We  know  of  no 
special  means  by  which  the  occurrence  of  endocarditis  can 
be  prevented  during  the  acute  stages  of  these  affections, 
other  than  the  ordinary  means  of  treatment  which  it  is 
advisable  to  adopt  for  the  treatment  of  the  primary  disease. 

It  is  especially  important,  as  Dr  Sansom  has  pointed  out, 
to  direct  attention  to  mild  cases  of  scarlet  fever,  measles,  and 
other  febrile  diseases  in  children,  and  to  protect  the  patient, 
more  especially  during  convalescence,  from  exposure  to  cold, 
and  the  other  exciting  causes  of  endocarditis.^ 

The  treatment  of  the  endocardial  inf  animation  zvhen  it  has 

'  Dr  Barlow  has  suggested  that  the  greater  frequency  of  mitral  stenosis  in 
young  women  than  in  young  men  may  be  due  to  the  fact  that  girls  suffer  much 
more  frequently  from  chorea  than  boys.  Be  that  as  it  may,  it  is,  I  think  probable, 
that  in  some  cases,  at  all  events,  the  endocardial  changes  established  during  an 
attack  of  chorea,  and  apparently  completely  recovered  from,  may  afterwards  be  the 
starting  point  of  serious  valvular  disease. 

'  Lettsomiafi  Lectures,  p.  t,i. 


396  Diseases  of  tJie  Heart. 

arisen. — Theoretically  our  first  indication  is  to  cut  short  and 
allay  the  inflammatory  process.  As  a  matter  of  practice  this 
indication  cannot  be  satisfactorily  carried  out,  for,  in  the 
first  place,  the  inflammation  has  already  made  considerable 
progress  before  it  can,  with  any  approach  to  certainty,  be 
recognised  ;  and  in  the  second  place,  we  cannot  bring  the 
depletory  and  other  local  measures  which  are  useful  in  the 
early  stages  of  most  inflammations,  to  bear  with  any  certainty 
upon  the  interior  of  the  heart. 

General  venesection,  the  internal  administration  of  tartar 
emetic,  and  other  remedies  of  a  similar  description,  which 
used  to  be  so  lavishly  employed  in  the  early  stages  of  internal 
inflammations,  are  especially  out  of  place  here,  for  one  of  the 
most  important  indications  which  we  have  to  carry  out  is  to  avoid 
anything  which  will  seriously  depress  the  action  of  the  heart. 

As  soon  as  rheumatic  endocarditis  is  distinctly  recognised, 
it  is  advisable,  as  Dr  Broadbent  has  pointed  out,  to  discon- 
tinue the  administration  of  salicylate  of  soda.  This  remedy 
docs  not  appear  to  possess  any  curative  action  so  far  as  the 
endocardial  inflammation  is  concerned,  and  it  does  seem  in 
many  cases  to  produce  cardiac  depression.  There  is  not, 
according  to  Dr  Maclagan,  the  same  (positive)  objection  to 
salicin,  which  may  still  be  continued  after  the  endocardial 
inflammation  is  recognised,  provided  that  the  joint  affection 
necessitates  its  use. 

It  is  of  the  utmost  importance  to  keep  the  heart,  so  far  as 
it  can  be  kept,  at  rest.  With  this  end  all  bodily  movement  ^ 
and  mental  excitement  must  be  avoided  ;  excessive  action  or 
irritability  of  the  heart  must  be  moderated,  and  for  this 
purpose  belladonna  and  digitalis  are  the  most  useful  drugs. 
Unless  the  joint  affection  continues,  the  pyrexia  is  seldom  suffi- 
ciently great  to  require  any  special  means  of  treatment.  For 
the  reduction  of  temperature  salicin  should  first  be  tried,  and  if 
that  drug  fails,  as  it  not  unfrequently  does  in  the  presence  of 
a  cardiac  complication,  recourse  must  be  had  to  quinine. 

In   the   majority  of  cases    this    treatment    is    all    that    is 

'  In  those  cases  in  which  the  joint  affection  still  continues,  the  patient 
instinctively  avoids  all  bodily  movement. 


T7'eatme?it  of  Acute  Endocarditis.  397 

required  in  addition  to  the  dietetic  and  other  measures  suit- 
able to  treatment  of  the  primary  affection. 

In  severe  cases,  when  the  valvular  apparatus  is  seriously 
damaged,  or  when  the  inflammation  of  the  endocardium  is  com- 
plicated with  pericarditis  or  with  myocarditis,  other  measures 
may  be  called  for.  One  of  the  most  important  indications 
in  bad — and  in  fact  in  all — cases,  is  to  look  out  for  symptoms  of 
cardiac  failure,  and,  when  nccessar}^,  to  strengthen  and  stimulate 
the  action  of  the  heart.  Digitalis,  brandy,  ammonia,  and 
ether,  are  the  remedies  which  are  most  useful  for  this  purpose. 

When  the  right  heart  becomes  seriously  embarrassed, 
local  depletion  by  means  of  leeches  is  often  most  useful.  But 
these  measures  will  be  more  particularly  detailed  when  I 
come  to  treat  of  valvular  lesions.     (See  p.  474.) 

Should  thrombi  form  in  the  cardiac  cavities,  the  internal 
administration  of  ammonia  may  be  tried,  as  first  recom- 
mended by  Dr  B.  W.  Richardson.  Ten  to  fifteen  drops  of  the 
liquid  ammoniae  may  be  given  internally  every  two  or  three 
hours  ;  or  ten  grains  of  the  carbonate  of  ammonia  may  be 
administered  in  a  table-spoonful  of  the  solution  of  the  acetate 
three  or  four  times  daily,  as  recommended  by  Bartholow. 

Embolic  and  other  complications  must  of  course  be  met 
by  appropriate  remedies  as  they  arise.  Space  does  not  allow 
me  to  go  into  details  here. 

ULCERATIVE   ENDOCARDITIS.^ 

Synonyms. — Septic  Endocarditis,  Infectious  Endocarditis, 
Diphtheritic  Endocarditis,  Endocarditis  Maligna  (Virchow), 
Arterial  Pyaemia  (Wilks). 

'  Professor  Osier  objects  to  the  tenii  'ulcerative,'  because,  on  the  one  hand, 
there  may  be  no  actual  ulceration  of  the  valves  in  cases  which  present  the  character- 
istic features  of  the  disease  during  life,  and  on  the  other,  endocardial  losses  of 
substance  may  occur  without  these  symptoms.  I  have  retained  the  term,  Jirsf/j/, 
because  it  is  the  title  most  generally  used  in  this  country-  ;  secondly,  because  ulcer- 
ation, though  not  invariably  present,  is  in  most  cases  a  characteristic  feature,  and 
represents,  so  to  speak,  the  highest  degree  of  development  of  the  local  lesion  ;  and 
thirdly,  because  the  term  represents  a  mere  pathological  fact,  and  does  not  suggest 
any  theory  as  to  the  causation  of  the  disease,  as  the  terms  septic,  infectious,  and 
diphtheritic  do — an  important  point  when  we  consider  the  difference  of  opinion 
which  exists  as  to  the  aetiology  and  pathology  of  the  affection. 


39B  Diseases  of  tJic  Heart. 

Definition. — An  acute  inflammation  of  the  endocardium, 
which  is  characterised,  pathologically — by  the  formation  of  fun- 
goid vegetations  and  (usually)  ulcerations  of  the  endocardium  ; 
clinically — by  great  prostration,  frequency  of  pulse,  fever  of 
an  irregular  or  suppurative  type,  symptoms  of  a  typhoid  or 
pyaemic  character,  together  with  enlargement  of  the  spleen, 
and  the  local  manifestations  of  embolic  infarctions  of  various 
organs.  The  invariable  termination,  so  far  as  at  present 
known,  is  in  death.  Micrococci  frequently  abound  in  the 
cardiac  vegetations. 

Aetiology. — There  is  considerable  difference  of  opinion  as 
to  the  nature  and  cause  of  ulcerative  endocarditis. 

Some  observers  regard  the  micrococci,  which  are  met  with 
in  the  cardiac  vegetations,  and  in  many  cases  also  in  the 
embolic  infarctions  of  distant  organs,  as  the  cause  of  the 
disease,  and  think  that  they  (the  micrococci)  gain  entrance 
into  the  blood  from  an  external  wound  or  an  abrasion,  or 
through  the  gastro-intestinal  tract  or  air  passages.  There 
seems  to  be  little  doubt  that  in  some  cases  the  cardiac  lesion 
is  simply  one  manifestation  of  a  general  pyemic  or  diphthe- 
ritic condition.  In  some  puerperal  cases,  for  instance,  as 
Rosenstein  points  out,  '  undoubted  diphtheritic  affections  have 
been  seen  in  the  mucous  membrane  of  the  uterus  and  vagina. 
And  in  these  very  cases  the  likeness  between  the  diphtheritic 
matter  found  on  the  genitalia  and  that  which  covers  the  endo- 
cardial abscess  is  so  strong,  and  parasitic  organisms  have 
been  detected  with  such  certainty  in  both  cases,  that  nothing 
but  the  most  stubborn  incredulity  could  deny  a  connection 
brought  about  by  the  blood,  between  the  affection  of  the 
genitalia  and  the  endocardial  centre.'  ^ 

Others,  while  admitting  that  micrococci  are  very  generally, 
if  not  invariably,  present  in  the  cardiac  lesion,  think  that  they 
are  rather  the  consequence  than  the  cause  of  the  affection,  or 
at  all  events  that  their  presence  is  accidental ;  in  other  words, 
they  believe  that  the  cardiac  vegetations  form  a  suitable  nidus 
in  which  the  micrococci  can  develop.     In  support  of  this  view 

'  Zlemssett's  Cyclojxcdia,  vol.  vi.  p.  70. 


Aitiology  of  Ulcerative  Endocarditis.  399 

they  state  that  micrococci  are  frequently  found  in  the  vege- 
tations of  rheumatic  endocarditis.  Osler,^  for  example,  who  is 
one  of  the  most  powerful  advocates  of  this  view,  states : — 
*  Micrococci  are  not  peculiar  to  the  vegetations  of  the  ulcerative 
form  of  endocarditis,  but  exist  in  the  small  beadlike  out- 
growths of  the  rheumatic  and  other  varieties  of  the  disease,  as 
Klebs  was  the  first  to  point  out.  My  experience  tallies  with 
his  ;  in  seven  specimens  of  verucose  or  plastic  vegetations 
which  I  have  examined  all  contained  micrococci.  ...  So 
far  as  my  observation  goes,  the  micrococci  do  not  exist  in  the 
blood  during  the  course  of  the  malady.  Nor  are  they  con- 
stantly found  in  the  infarcts.  The  occurrence  of  micrococci  in 
the  warty  vegetations  of  rheumatic  endocarditis,  and  in  the 
extensive  ulcerative  outgrowths  so  frequently  met  with  in  old 
sclerotic  valves,  are  facts  strongly  opposed  to  the  view  of 
their  specific  poisonous  nature.  The  micrococci  appear  to  be 
identical  in  these  cases,  though  Klebs  states  that  those  of 
rheumatic  endocarditis  are  larger  and  have  a  brownish  tint. 
I  cannot  say  that  these  differences  have  been  constant  in  the 
specimens  which  I  have  examined.  It  seems  a  pertinent 
question  to  ask,  if  in  the  malignant  form  of  endocarditis,  the 
micrococci  are  so  potent,  why  in  other  cases  in  which  they  are 
equally  prevalent,  should  they  be  inert }  Of  course  it  may  be 
urged  that  the  micrococci  may  be  of  different  kinds  or  pos- 
sess diverse  qualities,  or  that  the  resistance  offered  by  the 
tissues  to  their  penetration  varies  in  different  cases,  or  that  it 
is  only  in  weakened  and  debilitated  states  that  those  little 
bodies  thrive.  There  is,  I  think,  something  worthy  of  attention 
in  this  latter  view.  If  we  study  the  conditions  under  which 
endocarditis  develops,  we  find  almost  invariably  that  the 
patients  are  the  subject  of  some  other  constitutional  affection, 
which,  as  we  say,  predisposes  to  it.  What  determines  the 
precise  form  of  the  endocarditis,  we  do  not  know,  but  the  soft 
endocardial  vegetations  form  a  suitable  nidus  for  the  develop- 
ment of  micrococci.  They  appear  in  fact  to  be  just  as  much 
normal  components   of  endocardial   outgrowths  as  the   fibrin 

•    Transactions    of  the    Interiiatioual  Medical   Congress    of   Londoti,     1 88 1, 
P    345- 


400  Diseases  of  iJie  Heart. 

fibrils,  which  are  usually  deposited  and  among  which  the 
micrococci  abound.  It  is  evident  that  these  structures  are 
common  elements  in  a  series  of  endocardial  processes  which 
display  totally  different  symptoms  and  arise  under  different 
conditions.  How  far  they  are  responsible  either  for  the  de- 
velopment of  the  endocarditis  or  for  the  subsequent  characters 
which,  in  the  grave  form  it  assumes,  the  evidence  does  not,  I 
think,  warrant  as  yet  a  very  positive  opinion.'^ 

To  sum  up,  ulcerative  endocarditis  does  not  appear  to 
be  a  specific  infectious  disease  in  the  same  sense  that 
typhoid,  scarlet  fe\er  and  smallpox  are,  for,  so  far  as  I  am 
aware,  inoculation  experiments  have  failed  to  reproduce  the 
disease.  In  some  cases  the  endocardial  lesion  appears  to 
be  a  manifestation  of  a  general  p}-aEmic  or  diphtheritic  con- 
dition. In  these  cases,  an  unhealthy  wound,  diphtheritic 
ulcer,  or  diseased  patch  of  mucous  membrane,  is  the  original 
source  of  infection,  to  which  the  cardiac  lesion  is  secondary, 
though  the  infective  emboli,  which  become  detached  from  the 
cardiac  vegetations  and  ulcerations,  will  of  course  aggravate 
the  pyaemic  condition. 

In  other  cases  the  cardiac  lesion  is  the  primary  local  source 
through  which  the  system  becomes  impregnated.  This  group 
includes  cases  originating  in  the  course  of  acute  rheumatism 
and  old  standing  valvular  disease,  and  in  it  we  may  provision- 
ally include  those  cases  in  which  the  origin  is  obscure,  and  in 
which  the  primary  cause  of  the  endocarditis  is  unknown.  To 
these  cases  the  term  '  arterial  pyaemia,'  proposed  by  Dr  Wilks, 
seems  very  appropriate.  In  them,  owing  to  a  depraved  con- 
dition of  the  vital  forces,  and  of  the  heart  in  particular,  the 
resisting  power  of  the  tissues  is  diminished.  On  the  occur- 
rence of  endocarditis  (as  the  result  of  rheumatic  or  other 
causes)  micrococci,  which  we  must  suppose  are  always  cir- 
culating in  the  blood,  but  which  in  a  state  of  health  are  unable 
to  multiply  and  establish  themselves  in  the  tissues,  find  a  suit- 
able nidus,  and  develop  first  in  the  cardiac  vegetations  and 
subsequently   in    distant  organs  and   parts.     In   these  cases, 

'  Transactions  of  the  International  Medical  Congress  of  London,  l88r, 
p.  346. 


Etiology  of  Ulcerative  Endocarditis.  401 

the  cardiac  lesion  is  the  local  source  of  infection  through 
which  the  blood  becomes  poisoned  and  the  pyaemic  condition 
established. 

It  is  probable,  as  Dr  Murchison  has  suggested,  that,  in 
some  instances  in  which  the  symptoms  of  ulcerative  endo- 
carditis are  observed,  the  local  lesion  is  not  cardiac,  but  is 
situated  in  some  part  of  the  arterial  system. 

The  following  are  the  chief  conditions  with  which  ulcerative 
endocarditis  appears  to  be  associated  : — 

1.  Ac2ite  or  subacute  rheumatism. — The  exact  frequenc}^ 
with  which  this  association  occurs  has  yet  to  be  determined. 
Rosenstein's  view  that  the  majority  of  cases  of  ulcerative 
endocarditis  occur  in  the  course  of  acute  rheumatism  does  not 
appear  to  be  correct,  for  Osier  found,  on  analysing  the  reports 
of  fifty-seven  cases,  that  in  fifteen  only,  or  26.3  per  cent,  was 
any  mention  made  either  of  acute  rheumatism  or  of  previous 
rheumatic  attacks. 

In  the  rheumatic  cases  there  is  almost  invariably,  in  addi- 
tion, a  previous  history  of  ill  health  or  depressed  condition  of 
the  system  such  as  follows  want,  exposure,  the  abuse  of  alco- 
holics, etc. 

2.  Otd  standing  cardiac  disease  (valvular  lesions,  fibroid 
thickening  of  the  cardiac  walls). — It  is  probable  that  in  man}^ 
of  these  cases,  the  endocarditis  is  also  rheumatic,  A  depressed 
condition  of  the  system  seems  in  these  cases  also  to  be  an 
important  factor  in  determining  the  form  which  the  endo- 
cardial inflammation  ultimately  assumes.  The  low  organ- 
isation and  defective  vascularity  of  chronically  diseased  valves 
probably  also  favour  the  production  of  ulceration,  as  Virchow 
was  the  first  to  point  out. 

3.  Pyccuiia,  puerperal  fever,  dipJitJieria. — There  seems  to  be 
no  doubt,  as  I  have  already  mentioned,  that  in  some  cases  the 
endocardial  ulceration  is  only  one  manifestation  of  a  pyaemic 
condition,  which  has  its  original  source  of  infection  at  the 
periphery  in  the  shape  of  an  unhealthy  wound,  ulcerated  or 
diphtheritic  mucous  membrane,  etc.  In  the  majority  of  cases, 
however,  in  which  pyaemic  symptoms  are  associated  with  en- 
docarditis, the  sequence  of  events  is  probably  different,  the 

CC 


402  Diseases  of  t lie  Heart. 

cardiac  lesion  being  the  priman'  event  to  which  the  infection 
of  the  whole  system  is  secondary. 

4.  Injuries  iiiiattcndcd  with  local  suppuration. — Osier  has 
described  a  case  in  which  ulcerative  endocarditis  followed  a 
fractured  leg  (simple  fracture  unattended  with  local  suppur- 
ation), and  in  the  cases  which  he  anah'sed  he  found  a  con- 
siderable number  in  which  there  was  a  history  of  some  injuiy 
or  wound.  In  cases  of  this  description,  in  which  it  is  clearly 
proved  that  the  local  wound  or  injury  did  not  act  as  a  local 
source  of  pya^mic  infection,  we  can  only  suppose  that  the 
injury  had  a  depressing  influence  on  the  system  which  favoured 
the  production  of  the  ulcerative  rather  than  the  simple  form  of 
endocarditis,  the  endocardial  inflammation  being  probably 
due  to  some  other  condition  or  conditions. 

5.  Sypiiilis. — -In  some  of  the  recorded  cases  the  patient  suf- 
fered from  syphilis  before  the  onset  of  the  attack.  Possibly, 
therefore,  in  some  of  these  cases  the  endocarditis  was  in  the 
first  instance  syphilitic,  and  in  consequence  of  the  depraved 
condition  of  the  system,  and  low  resisting  power  of  the  tissues, 
it  assumed  the  ulcerative  form. 

In  addition,  there  remain  a  considerable  number  of  cases 
in  which  the  cause  of  the  condition  is  obscure. 

Age,  sex,  and  occupation. — Like  the  simple  form  of  endo- 
carditis, and  like  acute  rheumatism,  the  affection  seems  more 
common  in  young  than  in  old  people.  Males,  because  of  their 
being  more  exposed  to  depressing  external  influences,  alcoholic 
excesses,  etc.,  are  probably  more  liable  to  be  attacked  than 
females,  though  many  writers  state  that  the  liability  to  the 
affection  is  equal  in  the  two  sexes.  Persons  whose  occupa- 
tions necessitate  exposure  to  cold,  want,  and  other  injurious 
external  influences,  probably  suffer  more  frequently  than  other 
people,  but  no  particular  trade  seems  to  predispose  to  the 
disease. 

Pathological  anatomy. — In  the  majority  of  cases  the  left 
heart  is  the  chief  or  only  seat  of  the  lesion,  but  the  right  heart 
is  much  more  frequently  affected  than  in  simple  endocarditis. 

As  in  the  simple  form  of  inflammation,  the  valves  are  the 


%  X  ll     ^'  ^^ 


^^Ajl 


Fig.  168. 


"'^: 


jlortic  Valve  in  a  case  of  Ulcerative  Etidocarditis.  (^Natural  size.') 
The  Aortic  Cusps  are  thickly  coated  with  vegetations;  two  of  the  segments  are  ulcerated 
through  (pieces  of  whalebone  being  placed  in  the  apertures);  the  letter,  a,  points  to  a  small 
depression  (commencing  aneurism),  surrounded  by  minute  vegetations,  at  the  base  of  the  Aorta ; 
it  has  evidently  been  produced  by  the  vegetation,  b,  which  at  every  systole  would  be  forcibly 
washed  against  the  base  of  the  Aorta  at  this  spot. 


M<l«M«JCu««ii.cbi"cnoi 


Fig.  169. —  Vlceratlre  endocarditis;  Jfvjttvre  of  the  chordx  teiuUnex ;  Aneurisms  o»«  the 
mitral  valee.     (^\atiiral  size.) 

The  specimen  came  under  my  notice  iu  the  post-mortem  theatre  of  the  Eoyal  Itifirmary  of  Edin- 
burgh, during  the  winter  of  1883-84.  The  patient  was  under  the  care  of  Professor  Greenfield, 
with  whose  kind  permission  the  specimen  is  reproduced  here. 

A  piece  of  cane  has' been  passed  through  an  ulcer  in  one  of  the  aortic  cusps;  a,  a,  point  to 
two  ulcere  iu  the  anterior  flap  of  the  mitral  valve,  which  communicate  with  tlie  aneurisms  seen 
in  fig.  170;  6,  b,  ruptured  chordse  tenfliueaj.  Tlie  mitral  and  aortic  valve  segments  are  covered 
with  numerous  vegetations. 


Fig.  170. — Aneurisms  on  the  mitral  rnlve,  and  rupture  of  the  chordie  tendinese.     The  same  preparation 
rejyresented  in  Jig.  IGt*      (^Xatitral  size,  seen  from  behind.") 

a,  a,  aueurisms;  h,  b,  ruptured  chordae  tendincEe;  c,  c,  vegetatious  and  clots  attached  to  the 
chordffi  aud  papillary  muscles. 


Flo.  ITU'  —Aneurism  of  the  mitral  valre,  with  rupture  of  the  ralre  cusp.     Seen  fro7n  the  auricular 
surface.     {IJalfas  large  again  as  the  natural pre^mration .) 

a,  wall  of  left  auricle ;  b,  anterior  segment  of  the  mitral  valve,  the  chordae  tendinese  have 
been  cut  short;  c,  ineurism.     A  large  triangular  opening  is  seen  in  the  valve  segment. 

The  veutricular  surface  of  the  same  preparation  is  shown  in  fig.  171. 

(Copied  by  Professor  Turner's  permission,  from  a  specimen  in  the  Anatomical  Museum  of  the 
Edinburgh  University.) 


Fig  171  —Ulceration  of  the  anterior  segment  of  the  mitral  valve;  enorviotis  hypertrophy  anddilataUm 
of  the  left  ventricle ;  the  wrtic  valve  was  also  idcerated  and  highly  incompetent.  {Considerably 
less  tlian  the  actual  preimration  which  is  in  the  Anatomical  Museum  of  the  Edinburgh  University., 

The  anterior  segment  of  the  mitral  valve  has  been  turned  upwards  to  show  the  ventricular 
surface  of  the  valve.     A  piece  of  whalebone  is  inserted  in  the  perforation.  _ 

The  ventricle  lias  been  opened  from  behind,  and  its  walls  are  kept  apart  by  a  piece  of  stick. 
The  auricular  surface  of  the  ulcerated  valve  is  seen  in  fig.  170'. 


M'IjSAnICohMIhC  Ll'MC?  El 


Pathology  of  Ulcerative  Endocai'ditis.         403 

parts  of  the  endocardium  which  sufTcr  most,  but  the  hning 
membrane  of  the  cavities  is  much  more  frequently  impHcated 
than  in  the  simple  variety.  The  aortic  segments,  the  ven- 
tricular surface  of  the  mitral  valve  and  the  chordae  tendinese, 
are  also  more  often  found  diseased  than  in  simple  rheumatic 
endocarditis.  The  base  of  the  aorta  is  in  many  instances  also 
involved. 

The  extension  of  the  inflammatory  process  to  the  endo- 
cardium lininsf  the  cavities  of  the  heart,  and  to  the  linin"^ 
membrane  of  the  aorta,  is  generally  due  to  mechanical  causes, 
as,  for  example,  to  the  friction  of  a  vegetation  on  a  valve 
against  the  adjacent  wall  of  the  heart  or  aorta  (see  fig.  168), 
the  peculiar  limitation  of  a  layer  of  vegetation  and  fibrine,  on 
the  posterior  wall  of  the  left  auricle,  which  I  have  sometimes 
met  with,  is  another  example  in  point,  and  is  probably  pro- 
duced, as  Dr  Ashby  has  suggested,  by  a  regurgitant  current  of 
blood  passing  backwards  from  the  left  ventricle  and  causing 
an  inflammatory  condition  of  the  part  of  the  auricular  wall 
on  which  it  impinges  ;  in  other  cases,  as  I  have  previously 
mentioned,  the  position  of  the  lesion  is  determined  by  the 
presence  of  old  disease  (fibroid  thickenings)  which  render  this 
particular  part  more  liable  to  be  affected  than  the  surrounding 
healthier,  more  vascular,  and  more  resisting  tissue. 

The  most  characteristic  naked  eye  features  are  the  luxuri- 
ance of  the  vegetations  and  the  presence  of  ulcerations.  The 
vegetations  (see  figs.  168,  169,  174,  175)  may  be  of  all  sizes  and 
shapes  ;  they  are  usually  of  greyish  yellow  colour,  and  often 
present  a  granular,  fungating,  or  cauliflower  appearance ; 
occasionally  they  are  smooth  on  the  surface  ;  as  a  rule  they 
are  very  friable,  though  not  unfrequently  firmly  attached  to 
the  surface  of  the  endocardium  ;  quite  exceptional!}'  they  are 
tough  throughout. 

On  microscopical  examination,  the  base  of  the  vegetations 
is  found  to  consist  of  the  thickened  endocardial  and  sub- 
endocardial tissue,  in  which  granular  particles  and  micrococci 
sometimes  abound  ;  the  greater  mass  of  the  vegetations 
is  made  up  of  fibrine  and  granular  debris,  in  the  midst  of 
which  cellular  elements,  blood  corpuscles,  and  in  many  cases 


404  Diseases  of  the  Heart. 

immense  numbers  of  micrococci,  often  in  the  form  of  ball-like 
masses  (see  fig.  173)  arc  embedded. 


Fig.  173. — Ball-like  masses  of  Micrococci.     (Aflcr  Oskr.) 

The  edges  of  the  ulcers  or  erosions,  for  in  many  cases  they 
are  superficial,  are  uneven  and  granular.  The  base  of  the 
ulcer  has  usually  a  dirt)'  greyish-yellow  appearance,  and  to  it 
small  blood-clots  often  adhere.  The  subjacent  tissues  are 
always  more  or  less  extensively  implicated.  The  surrounding 
portions  of  the  endocardium  are  studded  with  projecting  gra- 
nulations and  vegetations,  in  many  cases,  in  fact,  the  ulcers  are 
hidden  beneath  the  fungating  growths  which  surround  them. 

When  an  ulcer  involves  a  valve  flap,  the  resisting  power 
of  the  membrane  is  of  course  destroyed,  and  under  the  force 
of  the  blood-pressure  an  acute  aneurism  or  bulging  of  the 
valve  is  not  unfrequently  produced.  The  valvular  aneurisms 
vary  in  size,  but  are  seldom  larger  than  a  marble.  When 
the  anterior  segment  of  the  mitral  valve  is  affected,  the  aneur- 
ismal  sac  bulges  into  the  auricle,  the  orifice  of  the  sac  being 
situated  on  the  ventricular  surface  of  the  valve,  i.e.  the  surface 
on  which  the  blood  presses  during  the  contraction  of  the  left 
ventricle.  (See  figs.  169,  170,  171,  172.)  Aneurisms  of  the 
aortic  segments  bulge  into  the  cavity  of  the  ventricle,  the 
orifice  of  the  sac  being  situated  on  the  upper  or  arterial  surface 
cf  the  segment;  and  here  again  the  direction  which  the  sac 
takes  is  determined  by  the  blood  pressure.     The  aneurismal 


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Pathology  of  Ulcerative  Endocarditis.  405 

sac  not  unfrequently  ruptures,  and  a  perforation  of  the  valve 
segment  is  produced. 

In  some  cases,  more  especially  in  the  case  of  the  aortic 
valve,  the  free  margins  of  the  flaps  are  more  or  less  completely 
destroyed  by  the  ulcerative  process. 

When  the  ulcer  is  situated  on  the  surface  of  the  endo- 
cardium lining  of  the  cavities  of  the  heart,  different  results 
may  follow  in  accordance  with  its  position,  extent,  and  depth. 
In  some  cases,  an  acute  aneurism  or  bulging  of  the  heart  wall, 
or  of  the  septum  ventriculorum,  occurs.  In  rare  cases  the 
cardiac  wall  or  septum  is  completely  eroded,  and  a  rupture  of 
the  heart  or  a  communication  between  its  different  cavities 
(between  the  two  ventricles  for  instance,  when  the  ulcer  is 
situated  on  the  septum  ventriculorum)  is  established.  In  other 
cases  again,  in  which  an  abscess  forms  around  the  base  of  the 
ulcer,  the  inflammatory  process  may  make  its  way  right 
through  the  muscular  wall  of  the  heart,  inflammation  of  the 
pericardium  being  ultimately  produced. 

An  ulcer  at  the  root  of  the  aorta  usually  results  in  the  pro- 
duction of  an  acute  aneurismal  dilatation  of  the  vessel  at  the 
weakened  spot.  An  aneurism  of  this  description  is  generally 
of  small  size.  It  may  project  into  the  pericardium  or  into  the 
pulmonary  artery.  Occasionally  its  rupture  is  the  immediate 
cause  of  death. 

In  addition  to  the  cardiac  lesions  which  I  have  just  de- 
scribed, other  morbid  appearances  are  almost  invariably  pre- 
sent. Enlargement  of  the  spleen  is  always  observed  ;  the  organ 
is  in  some  cases  soft  and  pulpy,  similar  to  the  enlarged  spleen 
of  fevers  ;  in  others  it  contains  infarctions.  The  portion  of 
the  capsule  corresponding  to  the  infarctions  is  not  unfre- 
quently thickened  and  coated  with  a  layer  of  recent  lymph. 

Embolic  infarctions  and  their  results  (softening,  inflamma- 
tory deposits,  etc.)  are  almost  always  found  in  some  of  the 
peripheral  parts  {i.e.  the  parts  peripheral  to  the  heart,  such  as 
the  spleen,  kidney,  brain,  skin,  etc.).  In  fact,  one  of  the  most 
characteristic  features  of  the  disease,  both  in  its  pathological 
and  clinical  aspects,  is  the  frequent  occurrence  of  embolic 
infarctions — a  tendency  which  is  at  once  accounted  for  by  the 


4o6  Diseases  of  tJic  Heart. 

facts  that  the  vegetations  are  very  friable  and  easily  broken 
down,  and  that  products  of  ulceration  are  washed  away  by  the 
blood  stream  as  it  passes  over  the  floor  of  the  ulcers.  The 
particles  which  are  thus  detached  are  for  the  most  part  small, 
and  are  therefore  carried  to  the  smaller  arteries  and  capillaries, 
where  they  stick,  and  give  rise  to  local  inflammations  and 
septic  deposits,  in  which  micrococci  can  often  be  detected  on 
microscopical  examination.  In  some  cases  larger  portions  of 
the  vegetations  are  detached,  and  the  larger  arteries,  such,  for 
instance,  as  the  middle  cerebral,  are  obstructed. 

Inflammation  of  the  serous  membranes,  more  especially 
pleurisy  and  empyema,  are  not  uncommon. 

The  membranes  of  the  brain  are  sometimes  inflamed  ;  and 
extensive  haemorrhages  have  been  met  with  both  in  the  sub- 
stances of  the  brain  and  on  its  surface.  Aneurismal  dilata- 
tions of  the  cerebral  blood-vessels  have  also  been  observed.^ 

The  mucous  membrane  of  the  intestines  is  sometimes  in- 
flamed and  ulcerated.  Inflammatory  deposits  in  the  subcutane- 
ous tissues  and  purpuric  eruptions  on  the  skin,  both  of  which 
are  probably  due  to  embolic  plugging,  also  sometimes  occur. 

Acute  croupous  pneumonia  is,  according  to  Osier,  a 
frequent  complication.  The  exact  relationship  of  the  pneu- 
monia to  the  endocarditis  is  not  definitely  known,  but  both 
conditions  are  in  all  probability  due,  as  Osier  suggests,  to  one 
and  the  same  cause.  Small  abscesses  in  the  heart,  probably 
embolic,  are  also  observed  in  some  cases. 

Clinical  History. —  Different  cases  of  ulcerative  endo- 
carditis present  great  varieties  in  regard  to  their  individual 
symptoms  and  to  the  rapidity  of  their  course  ;  it  is  ex- 
tremely difficult,  therefore,  to  give  a  general  description 
applicable  to  all. 

The  onset  is,  as  a  rule,  sudden.  A  patient,  for  example, 
who  is  suffering  from  a  mild   attack  of  rheumatic  fever,  or 

'  All  of  these  lesions — the  meningitis,  which  more  frequently  involves  the 
hemispheres  than  the  base  of  the  brain,  the  cerebral  haemorrhages,  and  the 
aneurismal  dilatations  of  the  cerebral  blood-vessels, — are  probably  the  result  of 
emboli. 


Symptoms  of  Ulcerative  Endocarditis.  407 

who  is  the  subject  of  old  cardiac  disease,  or  whose  general 
health  has  for  some  time  previously  been  below  par,  without 
perhaps  any  definite  indications  of  disease  or  local  lesion,  is 
suddenly  seized  with  a  rigor  which  is  quickly  followed  by 
fever  and  grave  constitutional  symptoms,  which  I  shall  pre- 
sently describe.  Occasionally,  though  very  rarely,  the  onset 
is  gradual.  A  remarkable  case  of  this  description  is  described 
by  Bristowe,^  in  which  for  several  weeks  before  the  patient's 
admission  to  hospital  she  suffered  from  what  appeared  to 
be  intermittent  fever. 

Syinptonis. — Subjective  cardiac  sensations  are,  as  a  rule, 
slight  or  altogether  absent,  though  palpitation,  praecordial 
distress,  or  actual  pain  in  the  region  of  the  heart,  are  occa- 
sionally complained  of 

In  some  cases,  marked  shortness  of  breath,  independently 
of  any  obvious  pulmonary  cause ;  more  or  less  drops}-  ; 
extreme  pallor  of  the  countenance  ;  great  rapidity  of  the 
pulse  {i.e.  symptoms  due  to  deranged  action  of  the  cardiac 
pump),  together  with  characteristic  physical  signs  of  cardiac 
disease  (such  as — a  diastolic  aortic  murmur — a  systolic  mitral 
murmur  with  accentuated  pulmonary  second  sound  and 
evidence  of  engorgement  of  the  right  heart,  etc.),  are  so 
prominent  that,  notwithstanding  the  presence  of  fever  and 
other  grave  constitutional  symptoms,  which  are  characteristic 
of  the  typhoid  or  pyaemic  types  of  the  affection,  the  atten- 
tion of  the  observer  is  at  once  directed  to  the  heart. 

In  these  cases,  as  indeed  in  all  types  of  the  disease,  the 
spleen  is  more  or  less  enlarged,  and  generally  tender  to  the 
touch  ;  and  symptoms  due  to  embolic  infarctions  in  the 
kidney  (such  as  albuminous  or  bloody  urine  and  tenderness 
over  the  loins),  in  the  brain-  (paralysis,  delirium,  convulsions, 

'  British  Medical  Joitnial,  iSSo,  vol.  i.  p.  800. 

^  The  nervous  symptoms  which  are  of  such  frequent  occurrence  in  these  cases 
may  be  due  to  a  great  variety  of  different  lesions,  all  of  which  are  probably  in  the 
first  instance  due  to  embolic  infarction  of  the  cerebral  vessels.  Amongst  these 
the  following  are  some  of  the  chief:  —  Embolic  plugging  of  numerous  small 
vessels  ;  embolic  plugging  of  large  vessels,  as  for  instance  the  left  middle  cerebral ; 
extravasations  of  blood  into  the  substance  or  on  the  surface  of  the  brain  ;  inflam- 
mation of  the  cerebral  membranes. 


4o8  Diseases  of  the  Heart. 

headache,  coma),  in  the  skin  and  subcutaneous  cellular 
tissue  (purpuric  symptoms,  local  swelling  and  tenderness), 
or  in  other  parts — are  very  generally  observed  and  constitute 
extremely  striking  and  characteristic  features  of  the  case. 
Pneumonia,  pleurisy  and  empyema  are  common  complica- 
tions. I  am  in  the  habit  of  describing  these  cases,  in  which 
cirdiac  symptoms  and  signs  are  prominent,  as  the  cardiac  type 
of  the  disease.^ 

In  the  majority  of  cases,  the  cardiac  symptoms  and  signs 
are  altogether  thrown  into  the  back  ground  by  the  severity  of 
the  general  and  constitutional  symptoms.  Fever,  usually  of 
an  intermittent  or  markedly  remittent  type,  great  prostration 
and  depression,  marked  increase  in  the  rapidity  of  the  pulse, 
rigors,  profuse  perspirations,  enlargement  and  tenderness  of 
the  spleen,  enlargement  of  the  liver,  symptoms  due  to  embolic 
infarctions  and  secondary  inflammations  in  the  kidney,  brain, 
skin,  and  serous  membranes,  and  indications  of  general  blood- 
poisoning,  are  some  of  the  symptoms  which  are  most  fre- 
quently obser\-ed.  Lung  complications,  such  as  pneumonia, 
cedema,  etc.,  often  occur.  The  symptoms  sometimes  very 
closely  resemble  those  of  typhoid  fever,  and  cases  have  been 
repeatedly  sent  into  hospital  in  which  this  mistake  in  diagnosis 
has  occurred. 

In  these  cases,  which  arc  described  as  the  typJioid  type  oi 
the  disease,  the  fever  is  a  prominent  symptom  (ranging  from 
101°  up  to  105°,  106°,  107°  F.,  or  even  higher),  and  is  of  a 
remittent  rather  than  of  an  intermittent  type.  Vomiting, 
diarrhoea,  distention  of  the  abdomen,  tenderness  and  gurgling 
in  the  right  iliac  fossa,  and  eruptions  of  a  roseolar  and 
j)urpuric  character,  and  in  some  cases  resembling  more  or  less 
closely  the  characteristic  eruption  of  typhoid  fe\-er,  have  all 
been  observed.  The  spleen  is  found  on  examination  to  be  en- 
larged and  tender  to  the  touch.  The  symptoms  of  cardiac 
disease  are  not  prominent,  and  may  be  altogether  absent. 

'  Although  it  is  convenient  for  descriptive  purposes  to  divide  cases  of  ulcera- 
tive endocarditis  into  certain  definite  clinical  groups,  and  to  describe  cases  of  a 
cardiac,  typhoid,  pycrmic,  and  aguish  type,  the  reader  must  not  forget  that  this 
division  is  to  a  certain  extent  arbitrary.  There  is  no  sharp  line  of  demarcation 
between  these  ditierent  groups,  which  run  into  one  another  in  all  directions. 


Symptoms  of  Ulcerative  Endocarditis.  409 

The  physical  examination  of  the  heart  may  throw  Hght 
upon  the  case,  as,  for  instance,  in  those  cases  in  which  un- 
doubted evidence  of  organic  valvular  disease  (such,  for 
example,  as  a  diastolic  aortic  murmur),  is  detected  in  a 
person,  whose  heart  is  known  to  have  been  previously 
healthy.  But  in  many  cases  the  information  derived  from 
the  examination  of  the  heart  is  much  less  certain.  In  some 
cases  in  which  extensive  cardiac  lesions  have  been  found 
after  death,  no  murmur  was  detected  during  life.  In  others, 
and  these  perhaps  constitute  the  majority,  an  apex  systolic 
murmur  which,  as  we  have  previously  seen,  may  depend  upon 
many  different  conditions,  and  which  is  therefore  somewhat 
uncertain,  as  a  sign  of  organic  valvular  disease,  is  the  only 
physical  alteration  to  be  detected.  The  uncertainty — as  to 
the  significance  of  the  murmur — is  still  further  increased  if 
the  condition  of  the  heart  prior  to  the  present  attack  of 
illness  is  unknown.  In  cases  of  this  description,  the  pulse  is 
often  very  much  accelerated,  the  tongue  becomes  dry  and 
brown,  sordes  may  cover  the  lips  and  teeth,  there  is  often 
more  or  less  delirium,  in  many  cases  the  patient,  for  some 
time  previous  to  death,  lies  in  an  apathetic  or  semi-conscious 
condition,  the  evacuations  being  passed  involuntarily.  In 
short,  the  general  symptoms  are  those  of  the  typhoid  state. 
In  these  cases,  death  is  usually  preceded  by  coma. 

In  other  cases  of  ulcerative  endocarditis,  the  symptoms 
are  identical  with,  or  resemble  more  or  less  closely  those  of 
pysemia.^ 

In  these,  which  are  described  as  the  ' pyczmic  type'  of  the 
disease,  the  fever  is  intermittent,  and  presents  the  irregular 
ups  and  downs  which  are  so  often  met  with  in  connection 
with  internal  suppuration,  or  rather  with  the  absorption  into 
the  blood  of  repeated  doses  of  pus  or  poisonous  materials 
produced  from  pus.  The  temperature  may,  in  brief  periods  of 
time,  range  between  105°,  106°,  107°,  108°  F.,  or  even  higher 
on  the  one  hand,  and  97°,  96°,  95°  F.,  or  lower  on  the  other  ; 

'  I  have  previously  pointed  out  that  in  some  of  these  cases  the  cardiac  lesion 
is  a  secondary'  manifestation  of  pyaemia,  and  that  in  others  the  pysemic  condition 
follows,  and  depends  upon  the  endocardial  inflammation. 


4IO  Diseases  of  tJ.e  HearL 

and  repeated  variations  of  this  description  may  occur  in  the 
course  of  the  twenty-four  hours.  Rigors  and  profuse  perspi- 
rations are  very  prominent  in  these  cases.  The  complexion 
is  usually  pale  and  sallow,  or  it  may  be  slightly  jaundiced. 
Cardiac  symptoms  and  signs,  and  symptoms  due  to  embolic 
infarctions,  similar  to  those  which  have  been  previously  de- 
scribed in  speaking  of  the  other  t}'pcs  of  the  disease,  are  also 
met  with. 

In  exceptional  cases  the  attacks  of  fever  occur  at  regular 
intervals,  and  are  characterised  by  a  cold,  hot,  and  sweating 
stage  (the  'ague  type'  of  the  affection).  Dr  Murchison,  for 
example,  relates  the  case  of  a  patient  with  disease  of  the 
aortic  valves,  who,  for  three  months  before  his  death,  had 
daily  paroxysms  of  fever,  sometimes  commencing  with  a 
definite  rigor,  and  always  ending  in  copious  perspirations,  and 
whose  friends  were  so  satisfied  that  the  fever  was  ague,  that 
nothing  would  satisfy  them  until  the  case  had  been  treated 
with  large  doses  of  quinine.^ 

Duration  and  termination. — The  duration  of  different  cases 
varies  considerably.  In  some,  death  occurs  within  a  few  days 
from  the  commencement  of  the  attack  ;  in  others,  as  for 
example  the  case  mentioned  by  Murchison,  and  the  one 
represented  in  figure  i6S,  the  symptoms  progress  much  more 
slowly,  and  may  continue  for  one,  two,  or  even  three  months. 
The  termination,  so  far  as  is  at  present  known,  is  invariably 
fatal. 

Diagnosis. — From  the  description  I  have  given  of  the 
clinical  history  of  the  affection,  the  reader  will  readily  under- 
stand that  in  some  cases  the  diagnosis  is  attended  with  con- 
siderable difficulty. 

Cases  of  the  'cardiac  type'  are,  as  a  rule,  readily  recog- 
nised. The  two  conditions  with  which  they  are  most  fre- 
quently confounded  are  : — 

I.  Acute  simple  endocarditis. 

'  Lancet,  May  3,  1879,  p.  618. 


Diagnosis  of  Ulcei^ative  Endocarditis.  41 1 

2.  Chronic  valvular  disease,  complicated  with   a  specific 
fever  or  local  inflammation. 


The  differential  diagnosis  of  acute  simple  and  of  ulcerative 
endocarditis. — The  two  conditions  cannot  always  be  distin- 
guished, for  cases  are  sometimes  met  with  which  seem  to  be 
connecting  links  between  the  two  forms.  In  typical  cases 
there  is  of  course  no  difficulty. 

In  ulcerative  endocarditis,  the  rheumc.tic  indications  are 
much  less  frequently  present  than  in  the  simple  form  of  the 
disease;  while  the  general  constitutional  symptoms  are  usually 
much  more  severe.  The  physical  signs  undergo  more  rapid 
alterations,  and  evidences  of  grave  organic  disease — such,  for 
example,  as  a  diastolic  aortic  murmur — are  more  quickly 
developed.  The  fever  is,  as  a  rule,  higher,  and  is  much  more 
prone  to  assume  the  suppurative  type.  The  prostration  and 
rapidity  of  pulse  are  much  greater.  Rigors  are  common  in 
the  ulcerative,  but  rare  in  the  simple  form  of  endocarditis. 

Enlargement  and  tenderness  of  the  spleen,  albuminous  or 
bloody  urine,  though  they  may  occur  in  the  simple  form,  are 
vastly  more  frequent  in  the  ulcerative  variety. 

In  the  simple  form,  embolic  infarctions,  are  compara- 
tively seldom  met  with,  and  usually  obstruct  large  vessels  ; 
while  in  the  ulcerative  variety  showers  of  emboli  are  apt  to 
occur,  and  it  is  the  smaller  vessels  which  are  generally 
plugged. 

Typhoid  and  pyaemic  symptoms  are  common  in  the 
ulcerative,  but  rare  in  the  simple  form. 

Simple  endocarditis,  when  uncomplicated,  is  seldom  fatal  ; 
while  ulcerative  endocarditis,  so  far  as  is  at  present  known, 
always  terminates  in  death. 

The  differential  diagnosis  of  ulcerative  endocarditis  and  of 
chronic  valvidar  disease^  cojiiplicated  zuith  a  specific  fever  or 
local  inflamviation. — When  a  local  inflammation  or  fever  is 
actually  present,  in  addition  to  the  symptoms  and  signs  of 
cardiac  valvular  disease,  or  in  a  patient  who  is  known  to  have 
been   previously  affected  with  a  chronic  valvular  lesion,  the 


412  Diseases  of  the  Heart. 

diagnosis  may  be  very  difficult  or  impossible.  In  attempting 
to  decide  the  point,  we  must  ask  ourselves  whether  a  local 
inflammation  and  an  old  cardiac  lesion  would  satisfactorily 
account  for  the  symptoms,  not  forgetting  that  local  inflam- 
mations, such  as  pneumonia,  for  example,  are  frequently- 
present  in  ulcerative  endocarditis.  We  have  in  fact  to  weigh 
carefully  all  the  facts  of  the  case,  and  without  committing 
ourselv^es  dogmatically  to  either  view — for  the  evidence  in 
cases  such  as  we  are  at  present  considering  seldom  justifies 
such  a  course — endeavour  to  determine  to  which  side  the 
balance  of  probabilities  and  weight  of  evidence  incline. 

Even  after  we  are  satisfied  that  acute  endocarditis  is 
actually  present,  we  have  still  to  determine  whether  the  case 
is  one  of  ulcerative  endocarditis,  complicated  with  a  fever  or 
local  inflammation,  or  of  simple  endocarditis  associated  with 
similar  conditions.  This  point  wc  must  endeavour  to  deter- 
mine in  the  manner  described  abo\e. 

Tlic  differential  diagjiosis  of  ulcerative  endocarditis  and  of 
typhoid  fever. — Cases  of  ulcerative  endocarditis  are,  as  I  have 
previously  pointed  out,  often  mistaken  for  typhoid  fever.  In 
trx'ing  to  determine  whether  a  doubtful  case  is  one  of  the 
t\'phoid  type  of  ulcerative  endocarditis  or  of  true  typhoid 
fever,  the  following  points  must  be  taken  into  account : — 

1.  TJie  mode  of  onset  and  rapidity  of  course. — -Ulcerative 
endocarditis,  as  a  rule,  begins  more  abruptly,  and  progresses 
more  rapidly  than  true  typhoid. 

2.  The  character  of  the  temperature  chart. — In  ulcerative 
endocarditis,  the  steady  and  gradual  rise  by  stages,  which  is 
so  characteristic  of  typhoid  fever,  does  not  occur.  At  the 
height  of  the  disease  (ulcerative  endocarditis)  the  remissions 
are  usually  much  greater  than  in  typhoid,  and  intermissions, 
in  which  the  temperature  falls  to  or  below  the  normal,  not 
unfrequently  occur. 

3.  TJie  temperature  pulse  ratio. — In  the  earlier  stages  of 
typhoid  the  pulse  may  not  be  at  all  increased  in  frequency, 
although  the  temperature  is  considerably  above  the  normal. 
In  the  earlier  stages  of  ulcerative  endocarditis  there  is  usually 


Diagnosis  of  Ulcerative  Endocarditis.  413 

a  marked  increase  in  the  frequency  of  the  pulse,  quite  inde- 
pendently of  the  amount  of  the  pyrexia. 

This  point,  which  is  one  of  considerable  diagnostic  value 
in  the  earlier  stages  of  the  disease  cannot  be  relied  upon 
afterwards,  since  in  the  later  stages  of  typhoid  the  pulse 
frequency  becomes  greatly  increased. 

4.  The  condition  of  tJie  Jtcart. — In  the  great  majority  of 
cases  of  ulcerative  endocarditis  there  are  physical  signs  of 
valvular  disease  even  in  the  earlier  stages  of  the  attack.  In 
typhoid  fever,  mitral  regurgitation  is  frequently  met  with  in 
the  later  periods  as  the  result  of  relative  or  muscular  incom- 
petence, but  valvular  lesions  are  rarely  present  at  the  com- 
mencement. 

The  exact  character  of  the  valvular  lesion  is  also  of  im- 
portance, a  mitral  systolic  murmur  developed  under  observa- 
tion is  much  less  significant  of  ulcerative  endocarditis  than  an 
aortic  diastolic  murmur  developed  in  a  similar  manner. 

Two  sources  of  error  must  of  course  be  remembered,  viz. : 
— (i)  The  cardiac  lesion  may  be  an  old  one  complicated  with 
typhoid.  (2)  Acute  endocarditis  does  sometimes,  though 
very  rarely,  occur  in  the  course  of  typhoid.  But  notwith- 
standing these  sources  of  error,  the  presence  of  a  recent 
valvular  lesion  is  strongly  in  favour  of  ulcerative  endocarditis. 

5.  Diarrhea,  zvith  pea-sonp  stools,  tenderness  and  gurgling 
in  the  right  iliac  fossa,  rose  spots  on  the  abdomen,  are  on  the 
other  hand  strongly  in  favour  of  typhoid ;  they  do  occasion- 
ally occur  as  isolated  symptoms  in  ulcerative  endocarditis,  but 
are  rarely  associated  together  in  the  same  case. 

6.  Symptoms  of  embolic  infarctions  are  very  strongly  in 
favour  of  ulcerative  endocarditis, 

7.  Rigors  arc  much  more  common  in  ulcerative  endo- 
carditis than  in  typhoid  ;  the  prostration  in  the  earlier  stages 
of  ulcerative  endocarditis  is  usually  more  marked. 

The  differential  diagnosis  of  2dcerative  endocarditis  and  of 
pyceniia. — Ulcerative  endocarditis  may  result  from  pysemia, 
and  pyaemia  may  follow  ulcerative  endocarditis.  But  since 
the  termination  in  both  of  these  conditions  is,  so  far  as  we  at 


4 1 4  Diseases  of  the  Heart. 

present  know,  always  in  death,  the  point  is  one  of  little 
practical  importance,  and  need  not  therefore  detain  us. 

It  is  of  great  importance,  however,  to  remember  that 
constitutional  symptoms  identical  with  the  symptoms  of 
pyaemic  ulcerative  endocarditis  are  not  unfrequcntly  met  with 
in  cases  of  abscess  of  the  liver  or  other  large  internal  and 
localised  collections  of  pus. 

Cases  of  this  description  are,  as  a  rule,  distinguished 
without  much  difficulty.  Attention  is  to  be  directed  to  the 
condition  of  the  heart  on  the  one  hand,  and  of  the  liver  and 
other  internal  viscera,  liable  to  be  affected  with  suppurative 
inflammation,  on  the  other.  The  occurrence  of  embolic 
symptoms  is  very  strongly  in  favour  of  ulcerative  endocarditis. 
It  must,  however,  be  remembered  that  it  is  not  always  easy 
or  possible  to  distinguish  embolic  infarctions  and  secondary 
pysemic  abscesses,  which  may,  of  course,  be  developed  in 
the  course  of  hepatic  abscess  and  other  internal  suppura- 
tions. 

The  differential  diagnosis  of  ague  and  of  iilecrative  endo- 
carditis.— Although  cases  of  ulcerative  endocarditis  do  occa- 
sionally occur  in  which  the  fever  intermits  at  regular  intervals, 
there  is  little  difficulty  in  distinguishing  them  from  cases  of 
true  ague.  The  intermissions  are  seldom  so  regular  ;  the  con- 
stitutional symptoms  between  the  attacks  of  fever  are,  as  a 
rule,  much  more  considerable,  and  progressively  and  quickly 
increase  ;  quinine  is  powerless  to  arrest  the  paroxysms  ;  cardiac 
murmurs  are  almost  always  present  ;  showers  of  emboli  are  apt 
to  occur ;  and  the  termination  in  ulcerative  endocarditis  is  in 
death. 

Prognosis. — The  prognosis  is  quite  hopeless  ;  all  cases,  so 
far  as  we  at  present  know,  end  fatally. 

Treatment. — Quinine,  in  full  doses,  together  with  free 
stimulation,  should  be  tried,  and  the  usual  treatment  for 
pyaemia  adopted.  The  treatment  recommended  for  severe 
cases  of  simple  endocarditis  may  also  be  carried  out. 


Chronic  Diseases  of  the  Endocardium.  4 1  5 

CHRONIC   ENDOCARDITIS. 
Definition. — Chronic  inflammation  of  the  endocardium. 

Aitiology. — In  some  cases  chronic  endocarditis  follows 
acute  or  subacute  endocarditis  ;  in  others,  the  endocardial 
inflammation  is  developed  very  slowly,  gradually  and  in- 
sidiously {i.e.  is  chronic  from  the  first),  and  it  is  not  until 
grave  valvular  defects  have  become  established  that  its  pre- 
sence is  suspected  or  recognised. 

In  a  considerable  proportion  of  cases — more  especially 
when  the  mitral  valve  is  the  seat  of  the  lesion — the  endocardial 
inflammation  is  of  rheumatic  origin. 

In  others,  the  endocardial  changes — which  for  the  sake  of 
convenience  we  are  in  the  habit  of  describing  as  due  to 
chronic  inflammation — are  closely  allied  to,  or  are  identical 
with  atheroma.  In  cases  of  this  description,  the  aortic  valve 
suffers  much  more  frequently  than  the  mitral.^ 

Alcoholic  excess,  syphilis,  and  gout,  are  all  predisposing 
causes  ;  indeed  there  seems  to  be  little  doubt  that  in  some 
cases  the  endocardial  inflammation  is  directly  due  to  gout, 
and  some  observers  think  that  it  is  sometimes  directly  due  to 
.syphilis. 

But  of  all  the  causes  of  chronic  endocarditis,  strain  is 
one  of  the  most  important — chronic  inflammation  of  the 
aortic  valves  is,  in  some  cases,  caused  by  strain  ;^  strain 
is  one  of  the  great  causes  of  atheroma  and  atheromatous 
valvular  lesions,  while  the  all  important  influence,  which  in- 
creased cardiac  effort,  i.e.  strain,  has  in  perpetuating  rheumatic 
inflammation  of  the  mitral  valve  has  already  been  insisted 
upon. 

Morbid  Anatomy. — The  essential  feature  of  chronic  endo- 
carditis is  the  production  of  a  dense  tissue,  consisting  of  spindle 

'  These  two  causes  of  chronic  valve  disease  are  very  frequently  combined.  A 
valve,  for  example,  which  is  thickened  by  the  atheromatous  process,  is  often 
attacked  with  chronic  inflammation. 

"  V^ide  the  aortic  regurgitation  which  is  frequently  met  with  in  young  puddlers, 
'  strikers,'  and  others  who  follow  laborious  occupations,  in  which  sudden,  violent 
nuiscular  efforts  are  required. 


4 1 6  Diseases  of  iJie  Heart. 

cells  and  fibres  (see  figs.  176  and  1/6'),  in  the  midst  of  which 
calcareous  particles  are  frequently  deposited.  As  in  the  case 
of  acute  endocarditis,  it  is  the  valvular  apparatus  of  the  left 
heart  (segments,  annular  rings,  chordae,  and  papillary  muscles), 
which  chiefly  suffers.  In  some  cases,  the  valvular  orifice  is 
contracted  or  narrowed  by  sclerotic  changes  in  the  annular 
ring  at  the  base  of  the  valve.  In  others,  the  thickened  and 
rigid  segments,  which  may  be  fixed  together  and  adherent  at 
their  edges,  form  unyielding  projections  which  narrow  the 
valvular  aperture.  In  almost  all  cases — whether  the  orifice  is 
stenosed  or  not — the  loss  of  elasticity  in  the  valvular  apparatus 
(segments,  basal  ring,  chordae,  or  papillary  muscles),  prevents 
the  perfect  closure  of  the  valvular  aperture,  and  incompetence, 
therefore,  results.  In  short,  the  practical  effect  of  chronic 
endocarditis  is  to  produce  incompetence,  or  both  stenosis  and 
incompetence  (very  rarely  stenosis  without  incompetence),  cf 
one  or  other  or  both  of  the  valvular  apertures  of  the  left  heart ; 
in  other  words,  to  produce  a  chronic  valvular  lesion. 

But  since  valvular  imperfections,  more  especially  valvular 
incompetence,  frequently  result  from  other  causes  than  chronic 
endocarditis,  it  is  now  desirable  to  consider  chronic  valvular 
lesions  as  a  whole. 

CHRONIC   VALVULAR   LESIONS. 

Definition. — Under  the  head  of  chronic  valvular  lesions  it 
is  convenient  to  consider  all  valvular  defects,  other  than  those 
which  have  been  already  described  in  treating  of  acute  en- 
docarditis. (I  shall,  of  course,  describe  the  chronic  valvular 
lesions  which  so  frequently  follow  acute  and  subacute  endo- 
carditis, but  I  shall  not  repeat  what  has  been  said  with  regard 
to  these  lesions  during  their  acute  stages.) 

yEtiolojy. — By  this  definition  a  great  number  of  different 
pathological  conditions  are  included  under  the  head  of  chronic 
valvular  lesions,  viz. : — 

I.  T/ie  chronic  vatvular  tesions  due  to  congenital  defects  and 
matforniations,  and  to  diseases  of  intra-uterine  life.— In  some  of 
these  cases  the  defect  or  malformation  is  so  severe  as  to  cause 


m^?^mM^- 


:''aP*, 


> 


->  m 


^^ 


y 


Fig.  176. — Section  through  the  endocardium  and  adjacent  portion  of  the  myocardium  in  chronic 
endo-myocarditis.    (^Magnified  about  50  diameters.') 

e,J,he  thickened  endocardium  (the  part  to  which  the  letter  e'  points  is  more  highly  magnified  in 
fig.  176');  7w,  part  of  the  myocardium;  ot',  a  band  of  muscular  fibres  adjacent  to  thp  endocardium 
which  still  remains;  m",  muscular  fibres  in  the  centre  of  the  cardiac  wall;  p,  pigment  granules  (the 
remains  of  atrophied  muscular  fibres)  lying  in  the  midst  of  fibrous  tissue ;  b,  b,  large  blood-vessels. 


^. 


t^- 


.^y 


**^ 


^a^r 


#» 


Fig.  176'. —  Chronic  Endocarditis.    A  part  of' the  preparation  represented  in  Jig.  176, 
more  highly  magnified  (x'^JoO). 

a,  free  surface  of  endocardium ;  6,  6,  spindle  cells ;  c,  c,  corpuscles. 


Chronic  Valvular  Lesions.  417 

serious  symptoms  from  the  date  of  birth.  In  others,  the  con- 
dition is  so  trifling-  as  to  be  unattended  for  years,  or  possibly 
for  the  whole  period  of  life,  by  any  injurious  eiTects.  It  must, 
however,  be  remembered,  as  Dr  Peacock  has  pointed  out, 
that  malformed  valves  are  more  liable  to  be  attacked  by 
endocarditis  than  naturally  formed  ones. 

The  more  severe  forms  of  congenital  valvular  lesions  are 
very  generally  right-sided,  and  are  usually  accompanied  by 
other  abnormalities  in  the  heart,  such  as  a  deficiency  in  the 
septum  ventriculorum,  a  patent  foramen  ovale,  etc.  Stenosis 
of  the  pulmonary  artery  is  by  far  the  most  common  congenital 
valvular  lesion. 

2.  The  chronic  valvular  lesions  produced  by  trajiniatic 
causes,  such  as  violent  effort  or  external  injury.  In  most  of 
these  cases,  the  valve,  which  gives  way,  is  not  absolutely  sound 
at  the  time  of  the  accident,  but  is  weakened  by  previous 
disease  (endocarditis,  atheroma,  etc.).  Traumatic  ruptures  due 
to  strain  are  in  the  great  majority  of  instances  confined  to 
the  aortic  segments,  and  produce  incompetence  (not  stenosis) 
of  that  orifice. 

3.  The  chronic  valvular  lesions  which  result  from  chronic 
endocarditis  (either  chronic  from  the  first,  or  followiJig  acute  or 
subacute  endocarditis). — In  the  majority  of  cases  the  lesion  is 
left-sided  ;  and  the  mitral  valve  is  much  more  frequently 
affected  than  the  aortic.  A  combined  condition  of  stenosis 
and  incompetence  usually  results.  Simple  incompetence  {i.e. 
incompetence  without  stenosis)  sometimes  follows ;  simple 
stenosis  [i.e.  stenosis  without  incompetence)  is  rare. 

4.  The  chronic  valvular  lesions  d?ie  to  atheroma. — Here 
again  the  lesion  is  almost  invariably  left-sided,  the  aortic 
valve  being  much  more  frequently  involved  than  the  mitral. 
A  combined  condition  of  stenosis  and  incompetence  usually 
results.  Incompetence  of  the  aortic  orifice  occasionally  occurs 
without  stenosis,  but  stenosis  without  some  incompetence  is 
very  rare. 

5.  The  valvular  imperfeetions  which  result  from  '  relative' 
and  'muscular'  i)icompetence,  as  I  am  in  the  habit  of  terming 
regurgitation  due  to  simple  dilatation  or  defective  muscular 

D  D 


4 1 8  Diseases  of  the  Heart. 

closure  of  the  valvular  orifices.  Lesions  of  this  description 
affect  the  auriculo-ventricular  valves  (both  the  mitral  and 
tricuspid)  much  more  frequently  than  the  sigmoid. 

Auriculo-ventricular  regurgitation  may  theoretically  be 
cither  'relative'  or  'muscular,'  but  as  a  matter  of  fact  I 
believe  the  two  conditions  are  very  generally,  if  not  invariably, 
combined.  In  cases  of  this  description,  unless  there  is  some 
other  valvular  lesion  present,  such  for  example,  as  stenosis, 
the  result  of  chronic  endocarditis,  the  regurgitation  is  simple, 
i.e.  unattended  by  stenosis.  The  mitral  and  tricuspid  re- 
gurgitation which  occurs  in  chlorosis,  progressive  pernicious 
anaemia,  exophthalmic  goitre,  the  advanced  stages  of  fevers, 
etc.,  are  typical  examples  of  this  form. 

Aortic  incompetence  is  never,  of  course,  '  muscular.'  Re- 
lative incompetence  of  the  aortic  orifice  is  simple,  i.e.  un- 
accompanied by  stenosis.  Increased  aortic  tension,  general 
dilatation  of  the  base  of  the  aorta,  or  aneurismal  dilatations 
immediately  above  the  aortic  segments,  are  the  conditions 
which  produce  it. 

It  is  said  that  'relative'  incompetence  of  the  pulmonary 
artery  may  be  produced  in  the  same  manner  as  relative 
incompetence  of  the  aortic  orifice  (by  increased  pulmonary 
tension,  etc.) ;  but  no  case  of  this  description  has  come  under 
my  own  observation. 

Pathological  physiology. — Now  all  lesions  which  impair 
the  efficiency  of  the  valves,  i.e.  all  valvular  lesions  which  pro- 
duce incompetence  or  stenosis,  or  a  combination  of  these  con- 
ditions, interfere  with  the  steady  onward  passage  of  the  blood 
in  the  normal  direction,  and  tend  to  produce  anaemia  in  front 
(arterial  anaemia)  and  congestion  behind  (venous  plethora). 
I  say  tend  to  produce,  for,  as  we  have  previously  seen,  com- 
pensatory changes  in  the  heart  are  almost  invariably  estab- 
lished, which,  for  a  time  at  least,  restore  the  balance  of  the 
circulation. 

The  effects,  in  short,  of  all  lesions  which  impair  the 
efficiency  of  the  valves,  are  partly  mechanical  and  partly 
vital,  and  vary  with  :  — 


Paihology  of  Chronic  Valviilar  Lesions.        419 

1.  The  valve  zvJiicli  is  affected,  and  tlie  exact  nature  of 
the  lesion. — The  effects  which  are  produced  for  instance,  by 
mitral  stenosis,  both  upon  the  heart  and  upon  the  peripheral 
venous  and  arterial  systems,  and  hence  upon  distant  organs, 
are  very  different  from  those  which  result  from  aortic  regurgi- 
tation. 

2.  TJie  suddenness  of  the  lesion. — When  a  valvular  lesion  is 
quickly  established,  as,  for  example,  when  an  aortic  valve-cusp 
is  ruptured,  a  sudden  strain  is  thrown  upon  the  cavity  of  the 
heart  which  is  placed  immediately  behind  the  lesion.  In 
consequence  of  the  sudden  increase  of  the  blood-pressure, 
dilatation  of  the  cavity  is  (apt  to  be)  produced,  and  hyper- 
trophy is  only  subsequently  established.^ 

When,  on  the  contrary,  a  valvular  lesion  is  slowly  and 
gradually  established,  the  blood-pressure  behind  the  lesion  is 
very  gradually  increased.  The  muscular  wall  of  that  cavity 
of  the  heart  which  is  gituated  immediately  behind  the  lesion 
is  stimulated  by  the  gradually  increasing  blood-pressure ; 
and  provided  that  the  vitality  of  this  organism  as  a  whole, 
and  of  the  heart  in  particular  is  good,  the  increased  stimu- 
lation is  attended  (in  the  case  of  obstructive  lesions  at  all 
events)  with  the  production  of  a  slowly  developing  hyper- 
trophy, which  lor  a  time  keeps  pace  with  the  valvular  lesion 
and  counterbalances  the  defect.  In  the  case  of  obstructive 
lesions,  then,  which  are  slowly  and  gradually  established, 
hypertrophy  of  the  cardiac  wall  behind  the  lesion  is  gradually 
produced,  and  it  is  only  subsequently  that  dilatation  is  set 
up.  This  statement  applies  more  especially  to  aortic  stenosis, 
for  in  the  case  of  the  mitral  valve  the  strain  on  the  thin 
walled  auricle  is  probably  from  the  first  attended  with  some 
dilatation.  We  shall  afterwards  see  that  in  the  case  of  re- 
gurgitant lesions  the  tendency  to  the  production  of  dilatation, 

'  In  the  lower  animals  artificial  lesions  of  the  valves  are  immediately  compen- 
sated by  the  reserve  force  which  the  heart  possesses.  In  the  human  subject 
lesions  of  this  description  seldom  occur,  except  in  the  caee  of  valves  previously 
weakened  by  disease  ;  and  in  such  cases  very  serious  derangement  of  the  circula- 
tion is,  as  a  rule,  immediately  set  up.  In  other  words,  the  reserve  force  possessed 
by  the  human  heart,  is  seldom  sufficient  to  coviplctcly  and  immediately  remedy  such 
a  sudden  and  severe  lesion. 


420  Diseases  of  the  Heart. 

in  the  earlier  stages,  is  even  greater  than  in  cases  of 
stenosis  ;  for  the  increased  blood-pressure  during  diastole, 
while  it  undoubtedly  stimulates  the  flaccid  muscular  wall  to 
contract  more  rapidly  than  is  natural,  tends  also  to  produce 
dilatation.  In  regurgitant  lesions,  then,  which  are  slowly 
and  gradually  established,  some  dilatation  in  addition  to 
hypertrophy  is  usually  produced,  even  in  the  early  stages  of 
the  case. 

3.  The  extent  of  tJic  tcsion. 

4.  The  general  vitality  of  the  individual  and  the  special 
vitality  of  the  heart  in  particidar.—li  the  general  tone  of 
the  organism  is  below  par,  and  more  particularly  if  the 
special  vitality  of  the  cardiac  muscle  is  interfered  with, 
either  as  the  result  of  defective  blood-supply  (disease  of 
the  coronary  arteries),  defective  nerve  supply,  or  structural 
defects,  such  as  fatty  or  fibroid  changes,  the  cardiac  muscle 
does  not  respond  to  the  increased  stimulation,  there  is  little 
or  no  compensation,  and  dilatation  and  not  hypertrophy  is 
produced. 

The  nctt  result,  then,  as  regards  the  mechanical  derange- 
ment of  the  circnlation,  which  is  produced  by  any  valvular 
lesion,  is  determined  by  the  suddenness  and  extent  of  the 
lesion  on  the  one  hand,  and  by  the  amount  of  the  com- 
pensatory changes  in  the  heart  on  the  other. 

When  we  come  to  measure  the  results  on  the  organism  as 
a  whole,  we  have  to  take  into  account  the  condition  of  the 
peripheral  organs  {i.e.  the  organs  peripheral  to  the  heart — 
the  centre  of  the  circulation).  The  same  amount  of  me- 
chanical derangement  of  the  circulation  will  produce  very 
different  effects,  for  example,  in  the  case  of  two  individuals, 
one  of  whom  is  healthy  and  the  other  in  a  state  of  disease. 
In  other  words,  the  resisting  power  to  the  mechanical 
derangement  of  the  circulation  possessed  by  the  peripheral 
tissues  and  organs,  more  particularly  the  condition  of  the 
digestive  apparatus,  the  kidneys,  and  the  nerve  centres,  is 
a  most  important  factor  in  determining  this  result. 

With  these  preliminary  remarks  we  will  now  consider  the 
lesions  of  the  different  valves  in  detail. 


Mitral  Iiicovifctcnce.  421 


MITRAL   INCOMPETENCE. 

Definition. — Mitral  incompetence  includes  all  those  con- 
ditions, which  interfere  with  the  perfect  closure  of  the  mitral 
valve  apparatus,  and  allow  a  regurgitant  blood  current  to  pass 
from  the  cavity  of  the  left  ventricle  to  that  of  the  left  auricle, 
during  the  ventricular  contraction  or  systole. 

Aetiology  and  PatJiology. — 'Mitral  regurgitation  is  a  very 
common  condition  ;  it  is  met  with  at  all  ages,^  and  in  a 
variety  of  affections,  and  may  result  from  a  lesion  of  any  part 
of  the  mitral  valve  apparatus  (sphincter  muscle,  basal  ring, 
valve  segments,  chordae  tendineae,  or  papillary  muscles) ;  but  in 
order  that  the  exact  manner  of  its  production  may  be  clearly 
understood,  I  must  direct  attention,  more  minutely  than  I  have 
hitherto  done,  to  the  construction  of  the  mitral  valve  appa- 
ratus, and  to  the  manner  in  which  its  closure  is  effected. 

The  function  of  the  mitral  valve  apparatus  is,  of  course,  to 
close  the  mitral  orifice  and  to  prevent  any  regurgitation  from 
the  cavity  of  the  left  ventricle  to  that  of  the  left  auricle, 
during  the  ventricular  systole.     This  closure  is  effected  : — 

(i)  By  the  narrowing  of  the  mitral  orifice,  which  results 
from  the  ventricular  cotitraction. 

The  mitral  orifice  is  surrounded  in  its  posterior  two-thirds 
by  the  muscular  fibres  of  the  left  ventricle  ;  while  the  anterior 
third,  which  is  fibrous,  is  formed  by  the  fibrous  continuation 
of  the  two  posterior  aortic  sinuses  to  which  the  great  anterior 
flap  of  the  mitral  valve  is  attached.  (See  figs.  177  and  178.) 
Now  during  the  ventricular  systole  the  muscular  fibres  sur- 
rounding the  mitral  orifice,  of  course,  contract  ;  and  (as 
Macalister  has  shown  in  the  admirable  lecture  in  which  he 
has  described  the  most  important  observations  of  Ludwig  and 
Hesse  on  the  form  and  mechanism  of  the  heart)  '  when 
systole  is  complete,  the  area  of  the  orifices  is  not  much  more 
than  half  of  what  it  is  in  diastole.'     (See  fig.  179.) 

'  Regurgitation  due  to  organic  changes  in  tlie  valve  segments,  which  is  gener- 
rally  due  to  rheumatic  endocarditis,  is  more  common  in  young  than  in  old  people. 


422 


Diseases  of  the  Heart. 


Fig.  177. — Portion  of  the 
aorta  and  wall  of  the  left 
ventricle  with  one  entire  seg- 
ment and  two  half  segments  of 
the  aortic  valve,  and  the  right 
or  anterior  segment  of  the 
mitral  valve;  a,  b,  c,  sinuses  of 
\'alsalva  opposite  the  seg- 
ments; in  a,  and  b,  the  aper- 
tures of  the  coronary  arteries 
are  seen ;  d,  cT,  the  inner  sur- 
face of  the  wall  of  the  ventricle  ; 
I,  2,  curved  attached  border 
of  the  segments  ;  3,  the  middle 
of  the  free  border  (corpus 
Arantii) ;  e,  e\  the  base  of  the 
anterior  segment  of  the  mitral 
valve;/,  its  apex;  between  t-, 
and  e' ,  and  /,  the  attachment 
of  the  branched  chordae  ten- 
dinece  to  the  margin  and  outer 
surface  of  the  valve  segment ; 
g,  right,  //,  left  principal  papil- 
lary muscle:  the  cut  chords 
tendineffi  are  those  which  be- 
long to  the  posterior  segment 
and  the  small  or  intermediate 
segments. — {After  Quain.) 


Fig.  178.— Calf's  heart  boiled, 
~li  .\\:ng  the  aortic  (C)  and  mitral 
I  1 1 '  rifices  thrown  into  one  by  the 
removal  of  the  mitral  valve,  the 
lower  A  being  the  central  fibro- 
cartilage,  E  the  tricuspid  orifice,  and 
F  the  orifice  of  the  pulmonary 
artery. — {After  Sibsoii.) 


yEliology  of  Mitral  lucoinpetcuce. 


Fig.  179. — Base  of  the  ventricles  in  systole  accordin'^  to  Luihvig ;   two-thirds 
natural  size. —  {After  Macalister. ) 


Fig.  180. — Cross  section  of  the  Tcntricles  in  systole. — (^After  Alacnlister.) 

(2)  By  the  acctirate  apposition  of  the  uiitral  segments. — 
There  are  two  mitral  segments.  The  ajtterior  flap,  which 
is  simple,  and   when   closed  is  shaped  like  a  three  quarters 


424  Diseases  of  t lie  Heart. 

moon,  '  is  attached  on  the  one  hand  to  the  junction  of  the  left 
ventricle  to  the  left  auricle,  and  on  the  other  to  the  roots  of  the 
right  and  left  posterior  flaps  of  the  aortic  valve.  This  attach- 
ment of  the  mitral  to  the  aortic  valve  is  effected  through 
the  fibrous  structure  that  extends  from  the  base  of  one  valve 
to  the  base  of  the  other,  and  by  the  central  fibro-cartilage  of 
the  heart,  which  forms  a  triple  bond  of  connection,  that  ties 
the  mitral,  the  aortic,  and  the  tricuspid  valves  to  each  other.' 
'  The  posterior  flap  is  compound,  and  when  closed,  is 
shaped  like  a  quarter  or  crescent-shaped  moon.  The  com- 
pound posterior  flap  is  usually  made  up  of  one  central  and 
two  lateral  sub-segments,  the  latter  being  sometimes  subdi- 
vided. These  sub-segments  adapt  themselves  so  to  each  other, 
that  the  concavity  of  the  crcscentic  border  of  the  posterior 
compound  flap  is  preserved  entire  ;  for  it  would  have  been 
impossible,  by  means  of  one  simple  fold  of  membrane,  to 
fill  up  without  a  break  the  whole  of  the  crescentic  border.' 
'  When  the  mitral  valve  is  shut,  the  anterior  flap  of 
the  valve  presents  a  convex  edge,  shaped  like  a  horse-shoe, 
which  falls  back  upon,  and  fits  like  a  lid  into,  the  posterior 
flap  of  the  valve,  which  flap,  being  crescentic  in  shape,  pre- 
sents a  concave  edge.  Each  flap  adapts  itself  to  the  other 
by  a  notched  lip,  made  up  of  small  hemispherical  eminences. 
The  eminences  of  one  lip  fill  up  the  notches  of  the  other  lip. 
These  eminences  thus  seen  on  the  auricular  surface  of  the  valve, 
are  cells  when  seen  on  its  ventricular  surface,  and  as  these 
cells  are  distended  with  blood  when  the  ventricle  contracts, 
and  are  exactly  maintained  in  their  places  by  the  tendinous 
cords  and  papillary  muscles,  the  distended  cells  or  eminences 
at  the  opposite  lips  of  the  valve  adapt  themselves  to  and 
press  against  each  other  during  the  systole,  so  as  to  shut  the 
valve.'^  (See  figs.  177,  181,  182,  and  183,  in  which  the  rela- 
tionship of  the  mitral  valve  segments  is  clearly  shown.) 

(3)  Further,  the  segments  of  the  valve  are  maintained  in 
position  by  means  of  the  cJiordce  tejidinece  and  papillary  muscles. 
— During    the  ventricular  contraction  shortening  of  the  pa- 

'  Sibson  on  the  Form  and   Position  of  the  Heart.     Russell  Reytiold's  System 
of  Medicine,  vol.  iv.  pp.  50,  51. 


Fig.  181. — Section  thvowjli  the  aorta,  left  auricle,  one  of  the  aortic  segmerrts  and  th&  anterior  cusp  of  the 
mitral  valve,  of  a  child  three,  iceeks  old.  (^Magnifed  about  10  diameters.)  The  aorta  has  become 
detached  from  the  auricle  iu  the  process  of  mouBting. 

a,  inner,  6,  middle,  and  e,  outer  coats  of  the  aorta;  c?,  sinus  of  Valsalva;  e,  segment  of  aortic 
valve ;y!y;  fat  cells;  ^,  r/',  cellular  tissue  hoiween  the  aorta  and  left  auricle,  whicli  have  become 
detached  In  the  process  of  mounting;  k,  endocardium  lining  tho  left  auricle;  i.  connective  tissue 
layer  of  the  endocardium  of  the  left  aiu'icle  ni.  in,  m,  muscular  fibres  of  the  \vall  of  the  left  auricle; 
n,  n,  anterior  segment  of  the  mitral  valve ;  >:,  placed  in  a  einus  or  depression  beneath  the  aortic 
valve  cusp. 


Fig.  182. — SeHirm  through  the  left  auricle  and  left  venlricie  of  a  child  three  weeks  old 
sliowinfi  the  attachment  of  the  posterior  segment  of  the  mitral  valve.  {Magnified 
about  10  diameters.) 

The  posterior  segment  of  the  mitral  valve  has  become  curled  up  in  the  process  of 
mounting;  the  relative  iliickuesses  of  the  endocardium  lining  the  auricle  and  ventiiole 
respectively  are  well  seen. 

a,  epithelial  covering,  aud 

b,  connective  tissue  layer  of  the  endocardium  of  the  left  aiu-icle ; 

c,  sub-eudocardial  connective  tissue 

d,  d,  muscular  fibres  of  the  left  auricle ; 

e,  connective  tissiie  of  the  outer  wall  of  the  left  auricle  aud  of  the  pericardium; 
y,  surface  of  the  pericardium  covering  the  left  auricle; 

g,  coronary  vein  transversely  divided; 

A,  pad  of  fat  between  the  auricle  and  ventricle ; 

i,  pericardium  covering  the  left  ventricle ; 

I,  large  vein  in  the  pericardium 

k,  k,  muscular  fibres  of  the  left  ventricle ; 

n,  the  turned  up  extremity  of  the  posterior  segment  of  the  mitral  valve; 

n',  the  point  of  attachment  of  a  chorda  teudiuea  to  the  mitral  valve. 


\M  M 


Fig.  W6.— Section  thromih  the  left  auricle  and  left  ventricle  of  a  child  three  weeks  old,  shmcinq  a  papillary 
muscle  and  its  chorda  in  ultn.  Marjnijied  abmit  10  dia7neters.  (The  perioardiiim  and  conuective 
tissue  oa  the  outer  surface  of  tfie  left  auricle  have  become  detached  in  the  process  of 
mounting.) 

/>, papillary  muscle;  c,  chorda  tendinea:  m,  posterior  segment  of  the  mitral  valve;  a,  wall  of  the 
left  auricle ;  v,  wall  of  the  left  ventricle. 


M=Uu.lCu«Ni»(iLi™c»Eoi 


y^tiology  of  Alitral  Licoinpetence.  425 

pillary  muscles  occurs,  and  in  consequence  of  this  shorten- 
ing the  various  parts  are  maintained  '  at  the  same  levels  in 
which  they  lay  in  diastole.'  ^  In  this  way  retroversion  of  the 
flaps  into  the  auricle  during  the  ventricular  systole  is  pre- 
vented. 

Regurgitation  or  incompetence  may,  therefore,  be  due  to 
the  following  pathological  causes  : — 

I.  Defective  musciilar  closure  of  tJie  valve.- — This  condition, 
which  I  term  muscular  incompetence,  and  which  is  very  often 
combined  with  dilatation  of  the  basal  ring  (relative  incompe- 
tence) is  a  common  cause  of  mitral  regurgitation.  Defective 
muscular  closure  is  produced  by  anything  which  impairs  the 
muscular  tone  of  the  left  ventricle  as  a  whole,  and  of  the  mus- 
cular fibres  which  surround  the  mitral  orifice  (the  mitral  sphinc- 
ter, as  I  term  it)  in  particular.  In  practice  we  find  this  form 
of  mitral  regurgitation  associated  with  : 

{a)  Chlorosis,  pernicious  ansemia,  and  other  anjemic 
conditions,  in  which  the  muscular  fibres  of  the  left  ventricle 
are  limp  and  fatty.  It  must,  however,  be  remembered,  that 
mitral  regurgitation  is  often  not  produced  by  the  fatty  degene- 
ration of  the  heart  which  occurs  in  old  people  — the  fatty  de- 
generation, for  example,  which  is  seen  in  connection  with 
disease  of  the  coronary  arteries  and  general  atheroma.  This 
apparent  exception  can,  I  think,  in  some  cases,  be  explained 
by  supposing  that  the  basal  tendinous  ring,  which  surrounds 
the  mitral  orifice,  is  thickened  or  even  calcareous  ;  and  that  in 
consequence  of  the  altered  condition  of  the  basal  ring  there 
is  stenosis  of  the  orifice,  or,  at  all  events  it  is  so  rigid  that 
dilatation  (relative  incompetence)  cannot  occur. 

ib)  Myocarditis,  more  especially  those  cases  in  which  the 
mitral  sphincter  is  involved.  I  have  already  alluded  to  this 
as  a  probable  cause  of  the  mitral  regurgitation  which  is  so 
common  in  acute  rheumatism.     (See  page  374.) 

ic)  The  degenerative  changes  in  the  cardiac  muscle  which 
are  met  with  in  the  later  stages  of  typhus,  typhoid,  and  the 
other  continued  fevers. 

'  Lecture  on  the  Form  and  Mechanism  of  the  Heart,  by  Dr  Donald  Macalister. 
British  Medical  Journal,  Oct.  28,  1882,  p.  825. 


426  Diseases  of  the  Heart. 

id)  Fibroid  degeneration  of  the  left  ventricle.  This  is  not  a 
frequent  cause  of  mitral  incompetence  \  firstly,  because  fibroid 
degeneration  of  the  left  ventricle  is  not  very  common  ;  and, 
secondly,  because  in  many  cases  in  which  the  left  ventricle  is 
affected  with  fibroid  degeneration,  the  conditions  for  the  pro- 
duction of  mitral  regurgitation  are  not  established.  If,  for 
instance,  the  mitral  sphincter  remains  sound,  or,  if  the  basal 
ring  is  narrowed,  as  it  often  is  in  consequence  of  the  endo- 
carditic  changes,  which  are  so  frequently  associated  wath 
fibroid  degeneration  of  the  wall  of  the  heart,  the  valve  flaps 
may  be  quite  competent  to  close  the  orifice. 

ie)  Grave's  Disease  (Exophthalmic  Goitre). — In  many  of 
these  cases,  mitral  regurgitation,  the  result  of  muscular  and 
relative  incompetence,  occurs. 

Stenosis  is  rarely  combined  with  '  muscular  '  and  '  relative  ' 
incompetence.  On  examining  the  heart  in  cases  of  this  de- 
scription, therefore,  after  death,  the  valve  may  appear  to  be 
perfectly  natural.  We  can  only^  judge  of  the  competence  of 
the  mitral  valve  (i)  by  accurate  measurement  of  the  orifice, 
and  (2)  by  careful  microscopical  examination  of  its  sphincter 
muscle.  And  in  judging  of  its  competence  by  measurement, 
it  is  important  to  remember  that  post-iiwrtcni  contraction 
of  the  left  ventricle  diminishes  the  size  of  the  orifice,  just  as 
ante-niortcvi  contraction  does. 

2.  Relative  Incompetence. — This  condition  is,  as  I  have 
mentioned  above,  generally  combined  with  'muscular'  incom- 
petence. It  occurs  more  particularly  in  those  cases  in  which 
the  cavity  of  the  left  ventricle  is  dilated  and  its  muscular  wall 
degenerated.  In  the  later  stages  of  aortic  regurgitation, 
mitral  regurgitation  due  to  a  combined  condition  of  '  relative ' 
and  'muscular'  incompetence,  is  of  common  occurrence."  High 
arterial  tension,  when  combined  with  impaired  tonicity,  fatty 
degeneration,  etc.,  of  the  left  ventricle,  also  gives  rise  to  it. 

'  The  water  test  is  useless  in  those  cases  in  which  the  left  ventricle  is  relaxed 
and  flaccid.  It  can  only  be  properly  applied  in  those  cases  in  which  the  heart  is 
in  a  condition  of  rigor,  and  the  left  ventricle  firmly  contracted. 

-  The  mitral  regurgitation,  which  is  sometimes  associated  with  increased  arterial 
tension,  is  in  other  cases  due  to  chronic  endocarditis,  set  up  by  the  violent  strain 
to  which  the  segments  are  sulijected. 


^'Etiology  of  Milral  Incompetence.  427 

3.  Structural  cJianges  in  tJie  valve  segments,  cliordiv  tenelineeE, 
and  papillary  muscles. -^Iw  cases  of  this  description  the  incom- 
petence is  very  generally  combined  with  more  or  less  stenosis 
of  the  orifice.^  The  incompetence  may  be  due  to  the  follow- 
ing conditions : — 

id)  Acute  Endocarditis. — This  cause  of  mitral  regurgita- 
tion has  already  been  fully  considered,  (See  page  371,  etseq.) 
It  will  be  remembered  that,  during  the  acute  stage,  the  in- 
competence is  generally ////r,  i.e.  unassociated  with  stenosis. 

{b)  Chronic  Endocarditis. — The  thickening  and  retraction 
of  the  valve  segments,  or  retraction  of  the  chordae  tendineae, 
prevent  the  accurate  apposition  of  the  valve  flaps,  and  re- 
gurgitation consequently  occurs.  Regurgitation  may  result 
from  elongation  and  stretching  of  the  chordae  tendineae,  which 
have  become  softened  by  the  inflammatory  process.  The 
mitral  flaps  are  consequently  no  longer  held  in  accurate 
apposition,  but  are  forced  too  far  back  during  the  ventricular 
systole. 

{c)  Rupture  of  the  chordae  tendineae. — This  is  fortunately 
a  comparatively  rare  condition.  The  regurgitation  which  re- 
sults is  very  free,  and  the  symptoms  proportionately  severe. 
More  than  one  cord  may  give  way.  Rupture  of  a  perfectly 
healthy  tendinous  cord  probably  never  occurs.  In  the  cases 
which  have  come  under  my  own  observation  in  the  post- 
mortem room  (such  as  that  represented  in  figs.  169  and  170), 
there  have  been  well-marked  appearances  of  endocarditis. 

{d)  Fatty  and  fibroid  changes  in  the  papillary  muscles. 
— In  fatty  conditions  of  the  left  ventricle,  notably  in  progres- 
sive pernicious  anaemia,  the  papillary  muscles  are  implicated. 
They  are,  also,  frequently  the  seat  of  fibroid  changes.  In 
chronic  endocarditis,  for  example,  the  tips  of  the  papillary 
muscles  to  which  the  thickened  tendinous  cords  are  attached, 
are  very  frequently  involved,  and  in  some  cases  the  whole 
muscular  fibre  of  one   or   more  of  the  papillary  muscles   is 

'  Incompetence  due  to  organic  changes  in  the  valve  segments  is  frequently 
combined  with  regurgitation  due  to  '  muscular '  '  or  '  relative  '  incompetence. 
This  is  more  particularly  the  case  in  the  terminal  stages  of  the  disease,  when  the 
muscular  fibre  of  the  left  ventricle  has  become  degenerated. 


428  Diseases  of  tJie  Hea rt. 

replaced  by  fibrous  tissue.  In  both  of  these  conditions,  but 
more  especially  in  the  former  (for  in  fibroid  degeneration  of 
the  papillary  muscles,  the  chordae  tendineae  are  often  re- 
tracted) the  mitral  segments  are  not  held  accurately  in  posi- 
tion during  the  ventricular  contraction,  but  are  floated  too  far 
back  into  the  orifice  ;  regurgitation  consequently  results. 

{e)  Atheroma. — The  anterior  segment  of  the  mitral  valve 
is  occasionally  aff"ected  with  atheroma,  though  much  more 
rarely  than  the  aortic  cusps.  In  many  cases  the  atheroma- 
tous deposits  do  not  interfere  with  the  competence  of  the 
valve  ;  in  others  (and  in  these  cases  chronic  endocarditis  is 
usually  present)  the  valve  segments  become  thickened,  rigid, 
and  incompetent. 

Pathological  Physiology. — The  first  effect  of  mitral  regur- 
gitation is,  of  course,  to  allow  some  of  the  blood,  which 
ought  to  be  pumped  into  the  aorta  during  the  ventricular 
systole,  to  pass  back  into  the  left  auricle  ;  in  other  words,  to 
produce  more  or  less  engorgement  behind,  and  more  or  less 
anaemia  in  front  of  the  cavity  of  the  left  ventricle. 

The  second  effect  is  to  produce  a  series  of  changes  in  the 
heart  itself,  the  other  parts  of  the  circulatory  system,  and  in 
the  peripheral  organs  {i.e.  the  organs  peripheral  to  the  heart 
— the  centre  of  the  circulation). 

Some  of  these  changes  are,  as  I  have  so  repeatedly  pointed 
out,  eminently  salutary  and  compensatory  in  character;  others 
are  as  decidedly  prejudicial. 

The  extent  of  the  vascular  engorgement  behind,  and  of  the 
anaemia  in  front,  is  equal,  as  we  have  previously  seen,  to  the 
amount  of  the  regurgitation  less  the  degree  of  compensation  ; 
while  the  extent  of  the  tissue  changes  is  determined  by : — 

(i)  The  amount  of  the  vascular  derangement  {i.e.  of  the 
engorgement  behind  and  the  anaemia  in  front). 

(2)  The  vitality  or  resisting  power  of  the  tissues  as  a  whole, 
and  of  certain  special  organs,  such  as  the  liver,  stomach, 
kidneys,  and  nerve  centres,  in  particular. 

But  since  it  is  of  the  utmost  importance,  both  for  the  due 
comprehension   of  the   symptoms    and    for    the    purposes    of 


Pathology  of  Mitral  Incompetence.  429 

intelligent  prognosis  and  treatment,  to  understand  clearly  the 
exact  nature  of  these  changes,  we  must  consider  them  in 
further  detail. 

Effect  on  the  left  auricle. — The  regurgitant  current  passes 
into  the  left  auricle  during  its  diastole,  i.e.  when  its  walls  are 
flaccid,  and  meets  the  blood  current  which  is  being  poured 
into  its  cavity  by  the  pulmonary  veins.  The  cavity  of  the  left 
auricle  is,  therefore,  more  forcibly  and  more  rapidly  dilated 
than  in  health  ;  its  muscular  wall  is  more  frequently  and  more 
powerfully  stimulated  ;  it  contracts  more  frequently,  and  tends 
to  become  hypertrophied.  The  hypertrophy  is  seldom  great ; 
for,  in  the  first  place,  the  muscular  wall  of  the  auricle  is  very 
thin,  and  is  much  more  easily  dilated  than  hypertrophied  ; 
and,  in  the  second  place,  the  primary  lesion,  which  produces 
the  regurgitation,  is  very  frequently  a  degenerated  or  debili- 
tated condition  of  the  ventricular  muscle.  In  cases  of  this 
description  {i.e.  cases  of  muscular  and  relative  incompetence) 
the  auricular  muscle  is  very  generally  in  a  similar  condition 
(degenerated  or  debilitated)  and  incapable,  therefore,  of  much 
hypertrophy. 

In  addition,  the  fibrous  layer  of  the  endocardium  lining 
the  auricle  usually  becomes  thickened.  The  usual  result  is, 
therefore,  that  the  cavity  of  the  left  auricle  becomes  more  or 
less  dilated,  its  muscular  wall  more  or  less  hypertrophied, 
and  the  fibrous  layer  of  the  endocardium  thickened. 

Now  all  of  these  changes  are  under  certain  circumstances 
salutary.  In  those  cases,  for  instance,  in  which  the  auricle 
becomes  just  sufficiently  dilated  to  accommodate  the  quantity 
uf  blood,  which  passes  back  at  each  ventricular  systole,  and  at 
the  same  time  to  receive  the  normal  quantity  of  blood  from 
the  lungs,  and  in  which  the  muscular  wall  of  the  auricle 
becomes  sufificiently  hypertrophied  to  expel  all  the  auricular 
contents  (both  the  blood  passing  into  its  cavity  from  the 
lungs  and  from  the  left  ventricle),  there  is  little  or  no  conges- 
tion behind  the  cavity  of  the  left  auricle,  and  the  lesion  is 
practically  compensated.  As  a  matter  of  fact,  such  perfect 
compensation  is  very  rarely  met  with,  except  in  those  cases 
in  which  the  regurgitation  is  small  in  amount,  and  in  which 


430  Diseases  of  t lie  Heart. 

the  vitality  of  the  cardiac  muscle  is  extremely  good.  Ex- 
amples of  such  perfect  compensation  do  however  occur, 
more  particularly  in  cases  of  mitral  regurgitation  in  which 
the  incompetence  is  caused  by  organic  changes  in  the  valve 
segments,  and  in  which  the  patient  is  young  and  healthy. 
Perfect  compensation  of  this  description  is  seldom  if  ever 
seen  in  'muscular'  or  'relative'  incompetence  or  \nfree  regur- 
gitation, the  result  of  organic  changes  in  the  valve  segments. 

Ejfects  on  the  Pulmonary  Circulation. — In  almost  all  cases 
of  mitral  regurgitation  the  pulmonary  circulation  is  obstructed. 
In  the  cases  of  perfect  compensation,  to  which  I  have  just 
referred,  the  obstruction  may  be  so  slight  as  to  be  practically 
ignored.  In  the  great  majority  of  cases,  it  is  much  more  con- 
siderable. The  free  passage  of  the  blood  from  the  pulmonary 
veins  into  the  cavity  of  the  left  auricle  is  interfered  with, 
more  particularly  during  the  period  of  the  ventricular  systole. 
The  tension  of  the  blood  in  the  whole  pulmonary  circuit  (the 
pulmonary  veins,  pulmonary  capillaries,  and  pulmonary  artery) 
is  consequently  increased.  Dilatation  of  the  pulmonary  ves- 
sels, more  especially  of  the  pulmonary  capillaries,  and  other 
secondary  changes  in  the  pulmonary  tissue,  to  which  I  shall 
presently  refer  more  in  detail,  occur. 

The  obstruction  in  the  lungs  during  the  ventricular  systole, 
throws  an  increased  strain  on  the  right  ventricle  of  the  heart, 
in  consequence  of  which  its  muscular  fibres  are  over-stimulated 
and  (when  healthy)  become  hypertrophied. 

The  dilatation  of  the  pulmonary  capillaries  is,  in  the  earlier 
stages  at  least,  seldom  so  great  as  in  mitral  stenosis,  for  in 
mitral  regurgitation  the  increased  blood  pressure  in  the  pul- 
monary circuit  is  not  so  continuous  as  it  is  in  stenosis  of  the 
mitral  orifice.  In  cases  of  mitral  regurgitation  (I  am  speaking 
of  comparatively  pjire  cases  in  which  there  is  little  or  no 
stenosis  combined  with  the  incompetence),  as  soon  as  the 
ventricular  systole  ceases,  the  mitral  valve  is  of  course  thrown 
open,  and  the  blood  pressure  in  the  pulmonary  circuit  is  sud- 
denly lowered.  In  mitral  stenosis,  on  the  contrary,  the  passage 
of  the  blood  from  the  left  auricle  to  the  left  ventricle,  through 
the  narrowed  orifice,  is  a  gradual  process  ;  and  the  fall  of  the 


PatJiology  of  IMilral  Incompetence.  431 

blood  pressure  in  the  pulmonary  circuit  is  much  more  slowly 
brought  about. 

It  must  also  be  remembered  that  in  mitral  stenosis,  and  in 
those  cases  of  mitral  regurgitation  in  which  the  muscular  wall 
of  the  left  ventricle  is  degenerated,  the  suction  action  of  the 
left  ventricle  is  much  less  perfect  than  normal,  and  the  passage 
of  the  blood  through  the  lungs  is,  from  this  cause,  rendered 
more  difficult  than  in  health.  In  the  healthy  condition  of 
things,  '  the  force  that  overcomes  the  resistance  of  the  lung 
capillaries  is  not  entirely  a  vis  a  tergo.  The  left  ventricle 
does  some  of  the  work  of  the  right.  To  produce  this  elastic 
straining  in  its  walls,  of  course  requires  a  greater  muscular 
effort  in  the  contraction  ;  but  the  energy  is  not  lost  or  wasted. 
When  diastole  begins,  it  is  restored— for  the  benefit  of  the 
pulmonary  circulation.' ^  In  those  cases,  therefore,  of  mitral 
regurgitation  in  which  the  ventricular  muscle  is  debilitated  or 
degenerated,  an  additional  strain  is  thrown  upon  the  right 
ventricle  in  consequence  of  the  diminished  suction  power  of 
the  left  heart  ;  vice  versa  in  those  cases  in  which  the  muscular 
wall  of  the  left  ventricle  is  healthy  and  hypertrophied,  the 
suction  power  of  the  left  heart  may  be  actually  increased,  and 
the  flow  of  blood  through  the  lungs  during  the  ventricular 
diastole  facilitated. 

Changes  in  the  right  heart. — As  I  have  just  explained,  the 
obstruction  to  the  passage  of  the  blood  through  the  lungs, 
which  results  from  mitral  incompetence,  throws  an  increased 
strain  on  the  right  ventricle  of  the  heart.  In  some  cases,  more 
especially  in  young  healthy  patients,  and  in  cases  in  which 
the  mitral  lesion  has  resulted  from  organic  changes  in  the  valve 
segments,  the  right  ventricle  responds  well  to  the  increased 
stimulation,  and  becomes  hypertrophied.  This  is  another 
eminently  favourable  and  compensatory  result.  Unfortu- 
nately, in  many  cases  (as,  for  instance,  in  all  those  conditions 
in  which  the  muscular  tissue  of  the  right  ventricle  is  debili- 
tated and  diseased),  the  response  is  imperfect,  and  dilatation, 


'  Lecture  on  the  Form  and  Ahrhiiiiisni  of  the  Heart,  by  Dr  Donald  Macalister, 
—  British  Medical  Journal,  Oct.  28,  18S2,  p.  S24. 


432  Diseases  of  tJic  Heart. 

or  a  combined  condition  of  dilatation  and  hypertrophy 
results.  In  proportion  as  the  dilatation  exceeds  the  hyper- 
trophy, so  is  the  result  injurious.  When  the  muscular  wall  of 
the  right  ventricle  is  debilitated,  and  when  the  cavity  of  the 
right  ventricle  is  dilated,  tricuspid  regurgitation,  as  the  result 
of  '  muscular'  and  '  relative'  incompetence  is  established,^  and 
the  last  barrier  which  protects  the  superior  and  inferior  venae 
cava;  and  the  veins  of  the  heart  itself,  from  the  baneful  effects 
of  backward  pressure,  is  removed. 

With  the  occurrence  of  tricuspid  regurgitation  the  cavity 
of  the  right  auricle  becomes  dilated,  the  fibrous  layer  of  its 
endocardial  coat  thickened,  and  in  some  cases  its  muscular 
wall  hypertrophied.  It  is  seldom,  however,  that  the  hyper- 
trophy is  sufficiently  great  to  be  of  any  practical  effect. 

Effect  on  the  left  ventricle. — Before  considering  the  results 
of  congestion  of  the  systemic  venous  circulation,  which  follow 
,  next  in  order,  as  we  proceed  backwards  from  the  mitral  valve 
to  the  periphery,  it  will  perhaps  be  well  to  direct  attention  to 
the  alterations  which  arc  produced  in  the  cavity  of  the  left 
ventricle,  and  to  the  conditions  which  result  therefrom. 

As  soon  as  the  systole  terminates,  the  elastic  recoil,  so  to 
speak,  of  the  left  ventricle  occurs  ;  the  mitral  valve  is  thrown 
open,  and  a  larger  quantity  of  blood  than  normal  passes  with 
unusual  force  from  the  cavity  of  the  left  auricle  into  that  of 
the  left  ventricle.  The  cavity  of  the  left  ventricle  is,  there- 
fore, more  quickly  distended,  and  its  muscular  wall  more 
powerfully  stimulated  than  in  health.  The  increased  stimula- 
tion, and  the  effort  which  is  required  to  expel  the  unusually 
large  quantity  of  blood,  result  in  the  production  of  hyper- 
trophy, in  those  cases  in  which  the  vitality  of  the  muscular  tissue 
is  good.  In  other  cases  {i.e.  when  the  vitality  of  the  cardiac 
muscle  is  impaired)  dilatation,  rather  than  hypertrophy,  occurs. 

'  Muscular  and  relative  incompetence  are  much  more  readily  established  at  the 
tricuspid  than  at  the  mitral  orifice.  This  is,  of  course,  just  what  we  would  expect, 
— the  muscular  wall  of  the  left  ventricle  being  so  much  more  powerful  than  that  of 
the  right.  The  condition  of  the  cardiac  muscle — its  capacity  of  becoming  hyper- 
trophied— is,  therefore,  a  most  important  factor  in  determining  the  progress  of 
mitral  regurgitation,  as  I  shall  afterwards  point  out  more  in  detail. 


PatJwlogy  of  Alitral  lucovipctcnce.  433 

In  consequence  of  the  hypertroph}',  the  left  \-entricle  is 
enabled  to  expel  a  larger  quantity  of  blood  than  it  otherwise 
could,  into  the  aorta  and  arterial  system.  In  this  respect, 
therefore,  the  hypertrophy  is  beneficial  and  compensatory. 
On  the  other  hand,  the  powerful  contraction  of  the  left 
ventricle  drives  an  increased  cjuantity  of  blood  through  the 
incompetent  mitral  orifice.  In  this  respect,  therefore,  the 
h}'pertrophy  is  bad. 

In  cases  of  mitral  regurgitation,  the  hypertrophy  is  seldom 
great,  and  is  usually  combined  with  more  or  less  dilatation  of 
the  ventricular  cavity.  In  judging  of  the  amount  of  hyper- 
trophy after  death,  it  is  important  to  note  the  condition  of 
the  muscular  fibre,  as  well  as  the  thickness  of  the  v/all  of  the 
ventricle  and  the  weight  of  the  heart.  Increased  thickness 
of  the  wall  of  the  ventricle  may,  of  course,  be  due  to  other 
conditions  than  increase  of  its  muscular  fibres  (such,  for 
instance,  as  fibroid  degeneration,  fatty  deposits,  and  thickening 
of  the  pericardium).  In  many  of  the  cases  of  mitral  regurgi- 
tation, in  which  the  muscular  fibre  becomes  hypertrophied, 
degenerative  changes,  such  as  fibroid  and  fatty  degeneration, 
subsequently  occur,  in  consequence  of  the  venous  hyperaemia 
in  the  cardiac  walls,  and  the  deficient  supply  of  healthy  arterial 
blood  resulting  from  an  advanced  mitral  lesion. 

It  must  also  be  remembered  that  the  hypertrophy  of  the 
left  ventricle  ma}'  be  due  to  extra-cardiac  causes,  such  as 
cirrhosis  of  the  kidney,  atheroma  of  the  arterial  system,  etc. 
It  is  also  probable  that  in  advanced  stages  of  mitral  disease, 
the  venous  engorgement  and  capillary  congestion,  by  impeding 
the  flow  from  the  arterial  to  the  venous  system,  throw  an 
increased  strain  upon  the  left  heart,  and  so  produce  hyper- 
trophy of  the  walls  of  the  left  ventricle. 

Effects  on  tlie  Systemic  I  ^enons  Circulation  and  PeripJicral 
Organs. — With  the  occurrence  of  dilatation  of  the  right  heart, 
and  more  particularly  after  tricuspid  incompetence  has  become 
fully  established,  the  systemic  v^enous  circulation,  which  is 
usually  from  the  first  more  or  less  interfered  with,  becomes 
seriously  embarrassed  ;  the  water}-  parts  of  the  blood  tend 
to  escape    into    the   subcutaneous    cellular   tissue   and    great 

E  E 


434  D/sc(7Si-s  of  the  Heart. 

lymphatic  sacs  (peritoneum,  pleurae,  pericardium),  and  the 
secondary  alterations,  which  the  venous  congestion  has  been 
slowly  producing  in  the  walls  of  the  heart  and  in  the  peripheral 
organs,  become  much  more  prominent. 

These  alterations,  which  are  partly  also  due  to  a  deficient 
supply  of  healthy  arterial  blood  are  of  the  greatest  practical 
importance,  and  must  be  considered  in  detail. 

Alterations  in  the  Lungs. — In  consequence  of  the  increased 
tension  of  the  blood  in  the  pulmonary  circuit,  the  pulmonary 
capillaries  become  dilated  and  encroach  more  upon  the  air 
space  (the  interior  of  the  air  vesicles)  than  in  health.  These 
thin  walled  and  dilated  vessels  are  easily  ruptured  by  any 
sudden  increase  of  the  blood  pressure,  and  hemoptysis  and 
pulmonary  apoplexy  are  therefore  apt  to  occur.^ 

The  venous  congestion  of  the  bronchial  veins,  which 
results  from  engorgement  of  the  systemic  venous  circulation 
leads  to  a  similar  change  (dilatation)  in  the  nutrient  vessels 
of  the  lungs  and  bronchi  ;  catarrh  of  the  air  vesicles  and 
bronchial  mucous  membrane  is  apt  to  arise,  and  the  condition 
which  has  been  termed  brown  induration  of  the  lungs  is  estab- 
lished. Gidema  of  the  lungs,  and  low  forms  of  pneumonia, 
are  also  very  apt  to  occur. 

Liver. — The  branches  of  the  hepatic  vein  become  dilated, 
and  the  liver  is  at  first  increased  in  size.  After  a  time  the 
liver  cells,  more  especially  those  in  the  centre  of  the  lobules, 
i.e.  in  the  zone  of  distribution  of  the  hepatic  vein,  become 
atrophied  and  fatt}'  ;  the  corpuscular  elements  of  the  blood 
(seen  after  death  in  the  form  of  pigment  granules  and  leu- 
cocytes) escape  from  the  dilated  and  congested  capillaries  into 
the  spaces  between  the  liver  cells.  Ultimately  the  organ  be- 
comes tougher  and  (sometimes)  smaller  than  normal,  and  after 
death  is  found  to  present  the  nutmeg  and  cirrhotic  appearance. 

Spleen. — The  spleen  becomes  engorged  and  enlarged  ; 
and  its  fibrous  stroma  increased.  After  death  it  is  found  to 
be  large,  tough,  and  of  a  dark  purple  colour. 

'  Haemoptysis  and  pulmonary  apoplexy  seldom  occur  in  the  early  stages  of 
mitral  regurgitation.  In  this  respect  mitral  incompetence  differs  from  mitral 
stenosis  in  which  spitting  of  blood  is  often  an  early  symptom. 


Pathology  of  Mitral  Incovipctcncc.  435 

Stoinacti  and  Intestines. — The  venous  radicles  and  capil- 
laries become  enormously  enlarged,  the  secreting  structures 
are  apt  to  become  atrophied,  and  a  catarrhal  condition  of  the 
mucous  membrane  established. 

Kidneys. — Chronic  congestion  of  the  kidneys  is  attended 
with  a  scanty  flow  of  high-coloured  urine,  which  deposits  a 
copious  sediment  of  urates  and  often  contains  albumen. 
After  death  the  kidney  is  found  to  be  firm,  tough,  and  dark- 
coloured.  A  form  of  cirrhosis,  in  which  the  organ  may  be  of 
normal  size  or  larger  than  natural,  is  ultimately  established. 

Pelvic  Viscera. — Chronic  venous  congestion  of  the  pelvic 
viscera  leads  in  the  female  to  leucorrha^a  and  derangements 
of  menstruation. 

Nerve  Centres. — The  venous  radicles  of  the  nerve  centres 
share  in  the  general  congestion  ;  the  nutrition  of  the  nerve 
elements  is  imperfectly  carried  on,  and  an  cedematous  con- 
dition, with  effusion  into  the  ventricular  system,  ultimately 
occurs.  The  impaired  nutrition  of  the  trophic  and  other  nerve 
centres,  reacts  upon  all  the  peripheral  organs  and  tissues,  and 
the  vitality  and  resisting  power  of  the  whole  organism,  includ- 
ing the  heart  itself,  become  seriously  impaired. 

Heart. — It  is  extremeh'  important  to  remember  that  the 
return  current  of  blood  through  the  cardiac  veins  is  also 
obstructed  ;  the  venous  radicles  and  capillaries  throughout 
the  heart  become  engorged  ;  their  contents  tend  to  escape 
into  the  lymphatic  spaces  between  the  muscular  fibres  ;  and 
the  nutrition  of  the  muscular  fibres  is  interfered  with.  After 
death  the  cardiac  walls  are  usually  found  to  be  tougher  and 
harder  than  natural.  In  those  cases  in  which  the  muscular 
fibres  are  fatty,  the  cardiac  wall  may  be  soft  and  pale. 

In  figure  184  I  have  attempted  to  represent  in  a  diagram- 
matic manner  the  effects  which  are  produced  in  the  peri- 
pheral organs  by  the  congestion  of  the  venous  system. 

Alterations  in  tlie  Composition  of  tJie  Blood. —  In  advanced 
stages  of  mitral  disease  the  composition  of  the  blood  is 
profoundly  altered,  and,  in  consequence  of  this  alteration,  the 
nutrition  of  the  tissues  and  organs,  including,  of  course,  the 
heart   itself,    is    very   imperfectly   carried    out.      The  altered 


436 


Diseases  of  the  Heart. 

\ 


Fig.   1S4. 


Clinical  History  of  Mitral  Licompctcncc.       437 

composition    of   the    blood    is    due    to    the    following    condi- 
tions : — 

I.  Imperfect  formation  and  elaboration. — The  appetite  is 
impaired,  the  amount  of  food  ingested  is  less  than  normal. 
The  functional  activity  of  the  stomach  and  other  organs, 
concerned  in  the  manufacture  of  the  blood,  is  seriously- 
damaged  in  consequence  of  the  deficient  supply  of  healthy 
arterial  blood,  and  of  the  venous  congestion  and  its  results, 
which  have  been  already  described.  The  impaired  functional 
activity  of  the  nerve  centres  reacts,  of  course,  upon  the  stomach 
and  other  chylopoietic  viscera,  and  adds  further  difficulties 
to  the  digestive  process  ;  2.  Imperfect  elimination  of  zvaste 
products. — The  functional  activity  of  the  liver,  kidneys,  in- 
testines, and  skin  is,  as  we  have  already  seen,  seriously  inter- 
fered with  and  the  blood  becomes  loaded  with  effete  products  ; 
3.  Imperfect  aeration. — In  consequence  of  the  imperfect  aera- 
tion of  the  blood  in  the  lungs,  which  is  one  of  the  most 
marked  features  in  advanced  cases  of  mitral  disease,  the  blood 
contains  a  larger  quantity  of  carbonic  acid,  and  less  oxygen 
than  usual;  4.  Loss  of  water  and  albumen,  which  occurs  in 
consequence  of  the  dropsical  effusions,  and  of  the  escape  of 
albumen  in  the  urine. 

Clinical  History. — Having  previously  described  in  detail 
the  clinical  history  of  mitral  regurgitation,  due  to  acute  endo- 
carditis, I  will  limit  the  following  remarks  to  the  chronic 
forms  of  the  disease.  And  in  considering  the  symptom- 
atology of  chronic  mitral  incompetence,  it  is  essential  to 
make  a  distinction  between  (i)  mitral  regurgitation  due  to 
organic  changes  in  the  valve  segments,  in  which  the  mitral 
lesion  may  be  said  to  be  the  primary  cause  of  all  the  sub- 
sequent symptoms,  and  (2)  mitral  regurgitation  due  to  other 
conditions,  such,  for  instance,  as  the  fatty  degeneration  and 
muscular  relaxation  of  chlorosis  and   progressive  pernicious 

Description  of  Fig.   184. 
Diagrammatic  representation  of  the  effects  of  a  mitral  lesion  upon  the  venous  circu- 
lation.    The  numbers  and  letters  are  the  same  as  in  fig  3.    (See  description 
page  5.)     The  arrows  indicate  the  direction  of  the  backward  current. 


438  Diseases  of  tJie  Heart. 

anaemia,  in  which  the  symptoms  are.  for  the  most  part,  due 
to  the  general  condition — in  chlorosis  and  progressive  anaemia 
— the  examples  which  I  have  taken — to  the  anaemic  condition. 

It  is  important  also  to  remember  that,  in  the  first  group 
of  cases,  associated  lesions,  such  as  aortic  valvular  disease, 
affections  of  the  kidney,  etc..  are  common,  and  complicate 
the  clinical  picture  of  the  case. 

Let  us  consider,  then,  in  the  first  place,  the  clinical 
history  of  the  chronic  mitral  incompetence,  which  is  due  to 
organic  changes  in  the  valve  segments.  The  symptoms  of 
this  condition,  which  usually  results  from  endocarditis  or 
atheroma,  and  which  is  generally  associated  with  some  con- 
striction of  the  valvular  orifice,  may  follow  the  symptoms 
of  an  acute  or  subacute  attack  of  endocarditis,  or  may  be 
very  slowly  and  gradually  developed  in  a  person  who  has 
previously  enjoyed  good  health. 

The  symptoms  vary  considerably  in  different  cases,  but 
are,  for  the  most  part,  due  to  mechanical  derangement  of 
the  circulation  in  the  peripheral  organs  {i.e.  in  the  organs 
peripheral  to  the  right  and  left  hearts).  Subjective  cardiac 
sensations  are  seldom  prominent.  In  advanced  stages  of  the 
case,  i.e.  when  the  dilated  cardiac  cavities  are  imperfectly  em- 
ptied, clots  sometimes  form  within  the  heart,  and  embolic  symp- 
toms due  to  the  plugging  of  distant  vessels  occasionally  arise. 

In  some  cases,  the  lesion  is  so  slight  and  so  perfectly  com- 
pensated, that  although  the  presence  of  a  permanent  apex 
systolic  murmur  indicates  to  the  medical  attendant  the  pre- 
sence of  mitral  regurgitation,  there  may  be  no  symptoms 
experienced  by  the  patient.  The  lesion  may  remain  in  this 
latent,  inactive  condition,  for  years.  In  some  cases,  it  neither 
interferes  with  the  comfort  of  the  patient,  nor  shortens  life. 

In  others,  and  these  are  the  majority,  there  is  shortness 
of  breath  on  any  extra  exertion,  while  dropsy  and  the  other 
symptoms  and  signs  of  a  progressive  mitral  lesion  are  ulti- 
mately developed,  and  lead  to  a  fatal  termination.  The 
occurrence  of  symptoms,  after  a  long  period  of  latency  or 
inactivity,  is  usually  due  either  to  a  subsequent  more  active 
development  of   the  \-al\-ular  lesion  as  the  result  of  chronic 


Symptoms  of  Mitral  lucompetcnce.  439 

endocarditis,  atheroma,  etc.,  or  to  the  failure  of  compensation. 
Both  of  the  conditions  are  particularly  apt  to  arise  between 
the  ages  of  fifty  and  sixt\',  when  the  degenerati\'e  processes  of 
old  age  and  decay  are  beginning  to  be  prominent. 

In  other  cases,  the  symptoms  gradually  progress,  it  may 
be  with  periods  of  temporary  compensation  and  intermission, 
from  the  time  when  the  patient  first  comes  under  obser- 
vation ;  and  after  a  longer  or  a  shorter  period,  which  depends 
upon  the  extent  of  the  lesion  and  the  vitality  of  the  indivi- 
dual, the  case  terminates  in  death. 

In  all  of  these  cases,  and  more  especially  in  the  last, 
urgent  cardiac  s}'mptoms  ma)'  be  suddenly-  developed,  and 
may  depend  upon  : — 

(i)  The  occurrence  of  acute  endocarditis. 

(2)  Rupture  of  the  tendinous  cords. 

(3)  Acute  pulmonary  complications  (such  as  acute  bron- 
chitis, pneumonia,  oedema  of  the  lungs,  pleurisy  with  effusion, 
etc.)  which  suddenly  add  to  the  difficulties  of  the  respiration 
and  to  the  engorgement  of  the  right  heart  and  of  the  venous 
circulation. 

The  first  symptoms,  which  patients  affected  with  mitral 
regurgitation  complain  of,  are  generally  due  to  engorgement 
of  the  pulmonary  vessels,  and  are  shortness  of  breath  on 
exertion,  going  up  stairs,  up  a  hill,  etc.  ;  and  slight  cough. 
As  the  case  advances,  the  shortness  of  breath  becomes  more 
marked,  and  the  cough,  which  is  sometimes  short  and  dry, 
at  others  accompanied  with  more  or  less  bronchial  secretion, 
becomes  more  frequent  and  troublesome. 

Palpitation,  intermittent  action  of  the  heart,  or  a  sinking, 
'  wanting,'  sensation  in  the  pit  of  the  epigastrium  are  some- 
times also  experienced.  Derangement  of  the  digestive 
organs,  loss  of  appetite,  foul  tongue,  flatulence  (which  by 
displacing  the  diaphragm  upwards  adds  to  the  mechanical 
difficulties  of  the  lungs  and  heart)  and  constipation,  or,  more 
rarely,  constipation  alternating  with  diarrhoea,  are  common 
even  at  comparatively  early  stages  of  the  case.  A  dingy 
colour  of  the  skin,  or  even  slight  jaundice,  and  piles  sometimes 
occur  at  this  stage  of  the  case.     The  patient  feels  depressed 


440  Diseases  oj  tlic  Heart. 

and  languid,  and  is  not  disposed  for  bodily  exertion  or  mental 
work.  A  close  observer  can  usually  detect  some  blueness  of 
the  lips,  ears,  nose,  fingers,  or  other  peripheral  parts  ;  and 
distended  congested  vessels  are  often  seen  coursing  over  the 
cheeks  and  sides  of  the  nose. 

After  a  time  the  stage  of  dropsical  effusions  is  reached, 
and  all  the  symptoms  become  more  prominent.  The  dropsy 
is  usually  first  observed  about  the  ankles,  and  only  at  night. 
As  the  case  progresses  it  becomes  permanent,  and  gradually 
extends  upwards.  The  subcutaneous  cellular  tissue  of  the 
lower  extremities,  scrotum,  and  dependent  parts  of  the  back 
may  become  enormously  swollen.  Effusion  also  takes  place 
into  the  internal  cavities,  more  particularly  the  peritoneum, 
pleurae,  and  pericardium.  When  the  mitral  lesion  is  com- 
plicated with  organic  renal  disease,  the  dropsy  may,  of  course, 
be  general.  When  again  cirrhosis  of  the  liver  is  associated 
with  mitral  regurgitation,  the  dropsy  into  the  peritoneal  cavity 
is  much  more  extensive  than  in  ordinary  cases  of  mitral  disease. 

The  shortness  of  breath,^  which  has  gradually  increased 
with  the  advance  of  the  cardiac  lesion  and  with  the  occurrence 
of  the  pathological  alterations  in  the  lungs  which  ha\e  been 
previously  described,  may  now  be  constant,  and  amount  to 
orthopnoea.  The  derangement  of  the  stomach,  liver,  and 
digestive  organs  becomes  greater.  Capillary  haemorrhages 
into  the  subcutaneous  tissues,  and  purpuric  eruptions  are 
commonly  observed  in  advanced  stages  of  the  case. 

The  nutrition  of  the  body  is  seriously  interfered  with  ;  the 
patient  loses  flesh  ;  the  number  of  red  blood  corpuscles  is 
diminished,  and  notwithstanding  the  cyanotic  condition  of  the 
periphery,  lips,  ears,  nose,  etc.,  a  condition  of  general  anaemia 

'  The  shortness  of  breath,  which  is  such  a  striking  feature  of  mitral  incom- 
petence, may  depend  upon  a  variety  of  causes,  amongst  which  the  following  are 
some  of  the  chief : — 

1.  An  increased  quantity  of  blood  in  the  lungs  requiring  oxydation,  and  a 
diminished  quantity  of  air  in  the  air  cells.  The  diminished  air  space  is,  to  some 
extent,  due  to  the  fact  that  the  dilated  pulmonary  capillaries  encroach  upon  the  air 
vesicles,  partly  to  the  chronic  catarrhal  condition  of  the  lungs  and  bronchi. 

2.  Secondary  changes  in  the  lungs  and  bronchi,  such  as  bronchitis,  emphysema, 
oedema,  pulmonary  apoplexy,  etc. 

3.  Secondary  changes  in  the  pleurnc,  such  as  hydrothorax,  pleurisy. 


Clinical  History  oj  Mitral  Incompetence.        441 

is,  to  some  extent,  established.  Tlie  urine  is  scanty  in  amount, 
high  coloured,  depositing  a  copious  sediment  of  urates,  and 
in  many  cases  containing  albumen.  The  functions  of  the 
nerve  centres  are  seriously  deranged  ;  in  some  cases  the 
patient  is  irritable  and  sleepless ;  in  others  drowsy.  Erythema, 
erysipelas,  or  even  gangrene  of  the  skin  of  the  swollen  (dropsi- 
cal) parts  is  apt  to  occur.  Spitting  of  blood,  the  result  of 
pulmonary  apoplexy,  is  of  common  occurrence.  The  respira- 
tion becomes  still  more  serio'usly  embarrassed.  Cheyne- 
Stokes'  respiration  may  occur,  and  after  a  prolonged  period 
of  terrible  suffering  death  takes  place. 

The  clinical  history  of  mitral  regiLrgitation,  due  to  initscitlar 
and  relative  incompetence,  need  not  be  specially  described.  In 
those  cases  in  which  the  debilitated  condition  of  the  cardiac 
muscle  depends  upon  a  general  pathological  state,  the  clinical 
picture  is  a  complicated  one.  In  some  cases,  the  symptoms, 
which  depend  upon  the  general  {i.e.  primary)  condition, 
entirely  overshadow  those  which  are  due  to  the  mitral  lesion. 
In  others,  the  reverse  holds  good  ;  in  chlorosis  and  progressive 
pernicious  anaemia,  for  instance,  shortness  of  breath  on 
exertion,  and  some  oedema  of  the  feet,  are  often  prominent 
symptoms.  Indeed,  I  have  known  more  than  one  case  of  this 
description  diagnosed,  and  that  by  no  incompetent  observer, 
as  primary,  organic,  mitral  disease.  The  distinctive  features 
of  these  and  other  cases  resembling  primary,  organic,  mitral 
disease,  will  be  presently  detailed. 

Physical  signs. — The  characteristic  physical  sign  of  mitral 
incompetence  is  a  systolic  murmur,  having  its  point  of  differ- 
ential maximum  intensity  at  the  left  apex  of  the  heart,  and 
its  direction  of  propagation  outwards  towards  the  left  axilla. 
(See  fig.  185.)  The  sound  characters  of  the  murmur  and  its 
extent  of  propagation  vary  very  much  in  different  cases,  and 
depend  upon  the  condition  of: — ■ 

(i)  The  left  ventricle. 

(2)  The  mitral  orifice. 

(3)  The  left  auricle. 


442  /J i senses  of  the  Heart. 

When  the  left  ventricle  is  hypertrophied,  and  its  muscular 
tissue  healthy,  when  the  mitral  orifice  is  partly  (though  not 


Fig.  1S5. — Outline  tigure  showing  point  of  difTerential  maximum  intensity  (*) 
of  the  systolic  mitral  murmur  (mitral  regurgitation);  and  the  direction  in  which 
it  is  propagated.  The  cross +  ,  which  is  supposed  to  represent  the  normal  position 
of  the  apex-beat,  is  placed  a  little  too  high. 

extremely)  constricted  and  its  edges  thickened,  and  when  the 
cavity  of  the  left  auricle  is  dilated,  the  most  favourable  con- 
ditions for  the  production  of  a  loud  and  extensively  con- 
ducted murmur  are  present.  In  cases  of  this  description, 
the  murmur  can  be  loudly  heard  in  the  back,  beneath  the 
inferior  angle  of  the  left  scapula.  ]^ice  versa  when,  as  in 
pure  muscular  incompetence,  the  wall  of  the  left  ventricle  is 
feeble,  and  when  the  annular  ring  is  dilated  rather  than  con- 
stricted, the  murmur  is  soft  and  faint,  and  is  badly  propagated. 
In  many  cases  of  this  description  it  cannot  be  heard  beneath 
the  inferior  angle  of  the  left  scapula. 

In  some  cases,  an  apex  s}'stolic  murmur,  indicative  of 
mitral  regurgitation,  can  of  course  be  heard  at  the  base  of  the 
heart  as  well  as  at  the  apex  ;  but,  for  the  reasons  previously 
given,  I  do  not  agree  with  Naunyn,  Balfour,  and  others,  who 
believe  that  a  s\-stolic  murmur,  haxing  its  point  of  maximum 


Physical  Signs  of  Mitral  1  iiconipeteiice.        443 

intensity  in  the  second  left  interspace,  at  a  point  an  inch  or 
an  inch  and  a  half  to  the  left  of  the  sternum,  and  which  is 
inaudible  at  the  left  apex,  is  indicative  of  mitral  regurgi- 
tation. 

In  those  cases  of  mitral  disease  in  which  the  heart  is  acting 
\-ery  quickly,  it  may  be  difficult  or  impossible  to  detect  a 
murmur.  When,  too,  the  left  ventricle  is  contracting  very 
feebly,  the  murmur  is  sometimes  absent.  In  those  cases  of 
organic  disease  of  the  valve  segments,  in  which  there  is 
stenosis  as  well  as  incompetence,  the  systolic  apex  murmur, 
indicative  of  regurgitation,  may  be  preceded  by  a  presystolic 
murmur  indicative  of  stenosis. 

In  addition  to  the  systolic  murmur,  which  can  be  heard 
with  the  ear,  a  systolic  thrill  can  sometimes  be  felt  when  the 
hand  is  placed  over  the  apex  of  the  heart.  This  sign  is  only, 
however,  present  in  a  minority  of  the  cases  of  mitral  incom- 
petence, and  even  when  present  is  not  of  very  great  practical 
importance,  for  in  those  cases  in  which  a  thrill  is  present,  a 
murmur  can  almost  invariably  be  heard.  A  thrill  is  in  favour 
of  the  case  being  one  of  organic  disease  of  the  valve  segments 
rather  than  'muscular'  or  '  relative'  incompetence. 

In  addition  to  the  systolic  apex  murmur  and  the  systolic 
thrill,  which  we  may  term  the  primary  physical  signs  of 
mitral  regurgitation,  other  physical  signs,  indicative  of  the 
secondary  changes  in  the  heart  and  circulation,  and,  therefore, 
of  the  greatest  importance  for  the  purposes  of  exact  diagnosis, 
prognosis  and  treatment,  are  met  with  in  most  cases. 

Amongst  the  secondary  physical  signs,  as  we  may  term 
them,  the  following  are  the  chief: — 

I.  Altered  character  of  the  radial  pulse. — The  modifications 
in  the  radial  pulse,  which  we  meet  with  in  mitral  regurgita- 
tion, depend  chiefly  upon  the  extent  of  the  lesion  and  the 
condition  of  the  left  auricle. 

The  frequency  of  the  pulse  is  increased,  for,  in  consequence 
of  the  leak  at  the  mitral  orifice,  the  left  auricle  is  more  quickly 
distended,  and  its  wall  is,  therefore,  more  repeatedly  stimulated 
than  in  health.  The  auricular  contraction  which  is  generated 
b\'    this    premature    stimulation    meets   with    no  obstacle    in 


444  Diseases  of  iJie  Heart. 

forcing  the  blood  through  the  mitral  orifice  ;  the  auricular 
contraction  passes  on  to  the  left  ventricle,  and  the  frequency 
of  the  pulse  is  increased.  The  volume  and  tension  of  the  pulse 
are  diminished  in  consequence  of  the  fact  that  some  of  the 
blood,  which  ought  to  be  passed  on  to  the  aorta,  passes  back- 
wards into  the  left  auricle.  The  extent  of  the  diminution 
depends  upon  the  extent  of  the  lesion  and  the  condition  of 
the  left  ventricle  ;  when  the  regurgitation  is  free  and  when 
the  left  ventricle  is  failing,  the  pulse  may  be  so  small  and 
feeble  as  to  be  almost  imperceptible  ;  vice  versa  when  the 
leak  is  slight  and  the  left  \-cntricle  healthy,  the  volume  and 
tension  of  the  pulse  are  not  much  modified.  The  rhythm  of 
the  pulse. — In  some  cases  the  pulse  is  quite  regular;  in  others, 
markedly  irregular.  These  differences  probabl}'  depend  to  a 
large  extent  upon  the  condition  of  the  muscular  \\alls  of  the 
heart.  So  long  as  the  muscular  fibres  of  the  left  auricle  and 
left  ventricle  are  healthy,  the  pulse  remains  regular,  or  the 
rhythm  is  only  slightly  altered.^  The  sphygmograyphic  charac- 
ters of  the  pulse  may  vary  considerably  in  different  cases  of 
mitral  regurgitation.  The  following  tracings  exhibit  some  of 
the  alterations  which  are  most  frequently  met  with.  (See  figs. 
1 86,  187,  and  188). 

2.  Accentuation  of  the  pulmonary  second  sound. —  In  free 
mitral  regurgitation  the  pulmonary  second  sound  is  accen- 
tuated in  consequence  of  the  increased  blood-pressure  in  the 
pulmonary  artery.  The  degree  of  accentuation  is  to  some 
extent  indicative  of  the  extent  of  the  mitral  lesion.  It  must, 
however,  be  remembered,  that  in  attempting  to  gauge  the 
extent  of  the  mitral  lesion,  by  the  degree  of  accentuation  of 
the  pulmonary  second  sound  which  is  present,  due  allowance 
must  be  made  for  the  facts  : — frstly,  that  increased  blood  pres- 
sure in  the  pulmonary  artery  may  be  due  to  any  obstruction 
in  the  lungs,  and  therefore  to  pulmonary  conditions  which  are 

'  Gaskell's  observations  as  to  the  alterations  in  rhythm,  which  result  from  modi- 
fications in  the  condition  of  the  cardiac  muscle,  quite  independently  of  alterations 
in  its  nerve  apparatus,  are  interesting  and  important  as  bearing  upon  this  point. 
It  must  however,  be  remembered  that,  in  man,  there  does  not  appear  to  be  any 
direct  connection  between  the  muscular  fibres  of  the  auricle  and  the  muscular 
fibres  of  the  ventricle,  at  the  auriculo-ventricular  ring.     (See  figs.  182  and  183.) 


Physical  Sigjis  of  Mitral  liicoinbeteiice.         445 

associated  with,  but  not  caused  by,  the  mitral  lesion  ;  secondly, 
that  the  loudness  of  the  pulmonary  second  sound,  even  in 
cases  in  which  there  is  great  obstruction  to  the  passage  of  the 
blood  through  the  lung,  the  result  of  advanced  mitral  disease 
or  any  other  condition,  depends,  to  a  considerable  extent, 
upon  the  condition  of  the  right  heart.  When,  for  instance, 
the  right  ventricle  is  feeble,  or  the  tricuspid  valve  incompetent, 
accentuation  of  the  pulmonary  second  sound  may  not  be 
observed. 


Pressure  3  oz. 
P'iG.  186. — Mitral  Regurgitation. — M.  A.  C,  cEt.  16,  admitted  to  Newcastle  In- 
firmary 24th  January  1878,  suffering  from  cough  and  shortness  of  breath, 
dating  from  an  attack  of  rheumatic  fever  two  months  previously.  Heart's 
action  very  rapid  (120-130).  The  first  sound  appeared  to  be  reduplicated  ; 
a  systolic  murmur  was  audible  at  the  apex  when  the  heart  became  slower. 


Pirssiire  4  oz 
Fig    187. — Mitral  Regurgitation. — S    13  ,  .vt.  58,  admitted  to  Newcastle  Infirmary 
25th   February   1878,   suffering  from   cardiac   dropsy.      There  was  a   well- 
marked  mitral  systolic  murmur,  which  disappeared  under  treatment.     The 
heart  was  considerably  enlarged  (hypertrophied  and  dilated). 


r, 


ressui  e  ,  oz. 


Fig  188. — Iireg'ilar  aiiit  /ti'eniiitteut  Pulse — O.  M.,  tvt.  40,  admitted  to  the 
Newcastle  Infirmary  suffering  from  cardiac  dropsy.  The  heart  was  very 
much  enlarged  ;  apex  beat  4^-  inches  below  and  3  inches  outside  left  nipple ; 
systolic  mitr.il  murmur. 

3.   Physical   signs    indicative   of    alterations    in    the    right 


446  Diseases  of  t lie  Heart. 

/;^^;-/._Hypertrophy,  dilatation  of  the  right  ventricle,  tri- 
cuspid incompetence,  and  dilatation  of  the  right  auricle,  are 
the  secondary  alterations  in  the  right  heart  which  may  be 
produced  by  a  mitral  lesion.  In  hypertrophy  of  the  right  ven- 
tricle, the  area  of  cardiac  dulness,  over  the  lower  end  of  the 
sternum  and  adjacent  costal  cartilages,  is  increased  ;  the 
impulse  of  the  right  heart  is  strong  ;  the  first  sound  of  the 
right  heart  long,  and  the  pulmonary  second  sound  loud.  In 
dilatation  of  the  right  ventricle,  the  area  of  cardiac  dulness 
over  the  lower  end  of  the  sternum  and  adjacent  interspaces,  is 
also  increased,  but  the  impulse  of  the  right  heart  is  feeble  ; 
the  first  sound  short  and  valvular,  or  replaced  by  a  systolic 
murmur  ;  when  tricuspid  incompetence  is  present,  the  second 
pulmonary  sound  may  not  be  accentuated.  In  tricuspid  in- 
competence, a  systolic  murmur  is  audible  in  the  tricuspid  area, 
and  when  the  incompetence  is  great,  true  jugular,  and  (in 
some  cases)  hepatic  pulsation  is  observed.  Dilatation  of  the 
right  auricle,  which  is  usually  associated  with  well  marked 
evidence  of  tricuspid  regurgitation,  may  give  rise  to  in- 
creased dulness  on  percussion,  and  in  some  cases  to  in- 
creased cardiac  impulse,  in  the  neighbourhood  of  the  third 
right  interspace. 

4.  Physical  signs  resulting  from  changes  in  the  left  ventricle. 
— In  free  mitral  regurgitation  there  is  usually,  as  we  have 
previously  seen,  some  hypertrophy  and  dilatation  of  the  left 
ventricle.  In  hypertrophy,  the  apex  beat  is  displaced  down- 
wards and  outwards  ;  the  area  of  cardiac  dulness  over  the  left 
heart  is  increased  ;  and  the  impulse  of  the  left  heart  is  strong  ; 
the  mitral  murmur  is  loud  and  well  propagated  ;  the  pulse  of 
fair  volume,  tension  and  regularity.  In  dilatation,  the  apex 
beat  is  also  displaced  downwards  and  outwards,  and  the  area 
of  dulness  over  the  left  ventricle  increased  ;  but  the  cardiac 
impulse  is  weak,  the  pulse  is  small,  feeble,  and  markedly 
irregular  ;  the  mitral  murmur  faint,  or  fin  some  cases) 
inaudible. 

The  characters  of  the  cardiographic  tracing  in  mitral  re- 
gurgitation differ  very  considerably  in  different  cases  and 
vary  with: — (i)  The  amount   of   the   regurgitation;    (2)  the 


Physical  Signs  of  Mitral  Incompetence.         447 

condition  of  the  left  auricle  (whether  hypertrophied  or  merely 
dilated) ;  and  more  particularly  (3)  the  condition  of  the  left 
ventricle,  whether  hypertrophy  or  dilatation  predominates.^ 

When  the  regurgitation  is  free,  and  more  especially  when 
it  is  uncombined  with  stenosis,  the  duration  of  the  diastolic 
portion  of  the  cardiac  tracing  is  shortened.  The  eminence  k 
is  usually  well  marked  ;  and  the  rapid  flow  of  a  large  quantity 
of  blood  from  the  over-distended  left  auricle  and  pulmonary 
veins  into  the  left  ventricle  may  be  manifested  by  a  rapid  ascent 
of  that  portion  of  the  tracing  placed  between  the  eminence  k 
and  the  rise  which  marks  the  commencement  of  the  ventri- 
cular systole.  In  those  cases  in  which  the  left  auricle  is 
hypertrophied  rather  than  dilated,  the  eminence  in  the  tracing 
which  represents  the  auricular  contraction  is  unusually  well 
marked. 

The  character  of  the  systolic  portion  of  the  tracing  depends 
upon  the  condition  of  the  left  ventricle.  When  hypertrophy 
predominates  over  dilatation,  the  breadth  of  the  systolic  por- 
tion may  be  considerable.  (See  fig.  191.)  When  dilatation  is  in 
excess,  the  summit  of  the  systolic  part  of  the  tracing  is  pointed, 
the  sudden  rise  which  corresponds  to  the  first  part  of  the  ven- 
tricular systole  being  followed  by  an  unusually  rapid  fall.  (Sec 
fig.  190.)  In  some  cases,  the  summit  of  the  systolic  portion 
of  the  tracing  is  double  or  forked.  (See  fig.  189.)  Dr  Sansom 
explains  this  forking  of  the  apex,  by  supposing  that  '  after  the 
first  ascent  of  the  lever,  due  to  the  hardening  and  rounding  of 
the  ventricle,  there  is  a  fall,  because  the  ventricle  has  lost  the 
point  d'appui  afforded  by  the  stretched  curtains  of  the  normal 
valve  ;  the  continuing  contraction  of  the  ventricle,  however, 
renews  the  elevation  at  the  end  of  the  systole."^  In  some 
cases,  the  regularity  of  the  systolic  portion  of  the  tracing  is 
interrupted  by  a  number  of  small  indentations  which  repre- 
sent the  vibrations  produced  by  the  regurgitant  blood  current. 
(See  fig.  1 89.)  In  many  cases  of  this  description  a  thrill  can  be 
felt  when  the  hand  is  placed  over  the  position  of  the  murmur. 

'  The  significance  of  the  difterent  portions  of  the  cardiographic  tracing  is  ex- 
plained in  the  appendix. 

-  Diagnosis  of  Diseases  of  fhc  Heart,  p.  2S4. 


448  Diseases  of  the  Heart. 

The  followini^"  tracini^s  represent  some  of  these  points:  — 


Fin.  1S9.  —  Cardiogram  is  a  case  of  mitral  regiirgilatton.  — [After  Sansoni.) 

'  a,  taken  at  tlie  exact  apex  ;  b,  taken  in  the  area  of  the  loud  systolic  murmur. 
The  iliastolic  portion  of  the  tr.icing  a  is  shortened  ;  the  summit  of  the  systolic 
portion  is  forked.  A  series  of  indentations  representing  the  sonorous  vibrations 
of  the  murmur  are  seen  in  h.'' — (Diagnosis  of  Diseases  of  tkc  Heart,  p.  283.) 


Vv;.   lyo.  Fig.   191. 

Fio.   190. —  Cardiograpliie  traeiiig  from  a  case  of  mitral  regurgitation  combined 
-.(litli  exophthalmic  goit)\'.  —  [After  Galabin. ) 
The  duration  of  the  diastolic  portion  of  the  tracing  is  shortenetl  ;  the  eminence 
k  is  prominent ;  the  auricular  impulse  a  present  ;  the  systolic  portion  is  indicative 
of  dilatation  of  the  left  ventricle. — [Guys  Hospital  Reports,  1875,  p.  314.) 

FiG.    191.  —  Cardiographic  tracing  from  a  case  of  mitral  regurgitation. 
—[After  Galabin.) 

'  A  loud  systolic  murmur  was  present  at  the  apex,  preceded  by  a  very  faint 
rumbling  sound.  A  presystolic  murmur  had  been  previously  heard.  The  heart 
was  much  hypertrophied.' — [Guys  Hospital  Reports,  1875,  p.  313.) 

5.  The  ph\'sical  signs,  which  result  from  altered  conditions 
of  the  peripheral  organs,  such  as  the  lungs,  liver,  stomach, 
spleen,  kidneys,  etc.,  need  not  be  detailed. 

Dia(^}iosis. — When  a  supposed  case  of  mitral  regurgitation 
comes  under  observation,  the  ph\-sician  has  to  inquire — 

Firstly,  If  the  mitral  valve  is  actually  incompetent.-* 

Secondly,  If  the  case  is  one  of  mitral  regurgitation,  is  the 
incompetence  due  to  muscular  or  relative  incompetence,  or  to 
organic  changes  in  the  valve  segments  } 

Tliirdty,  If  the  regurgitation  is  due  to  muscular  or  re- 
lative incompetence,  is  the  condition  curable  or  not  .' 


Diagnosis  of  Mitral  Incompetence.  449 

Fourthly.  If  the  regurgitation  is  caused  by  organic  changes 
in  the  valve  segments  what  is  the  extent  and  gravity  of  the 
lesion  ? 

Step  No.  I.     Is  the  mitral  valve  actually  incompetent  ? 

There  is  seldom  any  difficulty  in  deciding  this  point  ;  for, 
in  the  great  majority  of  cases  of  mitral  regurgitation,  a 
systolic  murmur,  having  its  point  of  differential  maximum 
intensity  in  the  mitral  area,  and  its  direction  of  propagation 
outwards  towards  the  left  axilla,  is  observed  ;  such  a  murmur 
is,  I  believe,  quite  characteristic  of  mitral  regurgitation.  Two 
sources  of  error  must,  however,  be  mentioned,  viz. : — 

(i)  The  murmur  may  be  ivanting  or  inaudible.— When 
the  left  ventricle  is  contracting  feebly,  the  regurgitant  blood 
current  is  not  sufficiently  powerful  to  produce  an  audible 
fluid  vein  or  murmur.  When,  again,  the  heart  is  contracting 
very  quickly,  it  may  be  difficult  or  impossible  to  detect  the 
murmur.  Now,  feeble  ventricular  contraction  and  very  rapid 
action  of  the  heart  are  frequently  observed  in  the  later  stages 
of  mitral  incompetence.  There  is,  however,  seldom  any  great 
difficulty  in  coming  to  a  correct  conclusion  as  to  the  nature 
of  such  a  case.  All  the  symptoms  and  signs  of  pulmonary 
and  systemic  venous  engorgement,  and  of  the  secondary  dilata- 
tion of  the  right  and  left  hearts,  which  I  have  previously 
detailed,  are  present.^  After  a  few  doses  of  digitalis  the 
frequency  of  the  heart's  action  is  lessened,  the  left  ventricle 
regains  power,  and  the  murmur  becomes  audible. 

(2)  The  murmur  may  be  simulated  by  other  murmurs. — 
Aortic,  tricuspid,  and  pulmonary  systolic  murmurs  can  usually 
te  distinguished  from  mitral  systolic  murmurs  without  diffi- 
culty. In  doubtful  cases  attention  must  be  particularly 
directed  to  : — the  exact  position  of  maximum  intensity  of  the 
murmur,  the  exact  direction  in  which  it  is  propagated,  the 
condition  of  the  right  and  left  ventricles,  and  the  characters 
of  the  pulse. 

'  Evidence  of  a  dilated  condition  of  the  left  heart  is  of  great  diagnostic  value  in 
cases  of  this  description,  which  are  very  closely  simulated  by  primary  lung  affec- 
tions with  secondary  alterations  in  the  right  heart  and  systemic  venous  circulation. 

F  F 


450  Diseases  of  tJic  Heart. 

Pericardial  inunnurs  audible  at  the  apex  can  usually  be 
distinguished  by  their  rhythm,  sound  characters,  area  of  dis- 
tribution, and  by  the  modifications  which  can  be  produced  in 
them  by  the  pressure  of  the  stethoscope.  Dr  Sansom  ^  states 
that  in  children  it  is  not  always  possible  to  make  the  distinc- 
tion. (Sec  also  table  III.,  page  330,^  in  which  the  differential 
diagnosis  is  further  set  forth.) 

Step  No.  2. —  The  ease  is  one  of  mitral  regurgitation  ;  is 
the  incompetejice  muscular  or  relative,  or  is  it  due  to  organic 
cha?iges  in  the  valve  segments  ? 

In  attempting  to  decide  this  point  it  must  be  remembered, 
that  the  two  conditions  (muscular  and  relative  incompetence 
on  the  one  hand,  and  incompetence  due  to  organic  changes  in 
the  valve  segments  on  the  other)  are  sometimes  associated  in 
the  same  case.  An  absolute  distinction  cannot,  therefore,  be 
made  in  every  case.  In  many  cases,  the  question  can,  how- 
ever, be  decided  with  considerable  or  absolute  certainty  ;  and 
this  step  in  the  diagnosis  is  one  of  the  greatest  practical  im- 
portance, for,  incompetence  due  to  organic  changes  in  the 
\alve  segments  is  a  permanent  condition,  whereas  regurgita- 
tion due  to  muscular  and  relative  incompetence  is  in  many 
cases  completely  curable.  As  a  matter  of  practical  experi- 
ence, we  know  that  this  question  presents  itself  for  solution, 
more  particularly  in  the  following  conditions  : — 

(i)  /;/  acicte  cases  attended  with  fever. — In  these  cases,  we 
have  frequently  to  decide  whether  an  apex  systolic  murmur 
is  due  to  acute  endocarditis  or  to  acute  relaxation,  so  to 
speak,  of  the  cardiac  muscle  (acute  muscular  incompetence). 

In  acute  rheumatism,  in  the  course  of  which  acute  endocar- 
ditis is  so  apt  to  arise,  it  may  be  very  difficult  or  impossible  to 
come  to  a  positive  conclusion,  as  I  have  already  pointed  out 
in  detail.     (See  p.  374.) 

In  other  febrile  conditions,  such  as  typhoid  and  typhus,  in 

the  course   of  which  endocarditis   is  rare,  but  acute   febrile 

degeneration  of  the  cardiac  muscle  common,  the  question  is 

more  easily  decided.     The  period  of  the  attack  at  which  the 

'  Lettsomian  Lectures,  p.  38. 


Diagnosis  of  Mitral  Incorupetence.  451 

murmur  is  developed,  and  the  presence  or  absence  of 
symptoms  indicative  of  mechanical  interference  with  the 
course  of  the  circulation,  are  the  points  to  which  attention 
must  be  particularly  directed  in  making  the  diagnosis.  When 
the  murmur  appears  late  in  the  disease  {i.e.  after  a  sufficient 
period  has  elapsed  for  the  production  of  acute  febrile  de- 
generation of  the  cardiac  muscle)  ;  when  there  are  no  distinct 
signs  of  mechanical  derangement  of  the  circulation,  such  as 
shortness  of  breath,  dropsy,  etc.  ;  and  when  there  are  no 
embolic  symptoms,  a  diagnosis  of  acute  muscular  incom- 
petence may  be  confidently  made.^ 

(2)  In  cJiorca  the  same  question,  i.e.  whether  a  mitral 
systolic  murmur  is  due  to  acute  endocarditis  or  to  muscular 
incompetence,  also  occurs.  But  I  need  not  further  refer  to 
this  point,  which  has  already  been  considered  in  detail. 
(See  p.  y-jz:) 

(3)  ///  many  chronic  affections. —  In  chronic  cases,  more 
specially  in  those  conditions  zvhich  are  associated  zvith  ancemia, 
the  question  constantly  arises  whether  a  systolic  mitral 
murmur  is  due  to  an  organic  lesion  of  the  valve  segments  or 
to  muscular  incompetence. 

In  some  cases  of  anaemia,  the  diagnosis  is  difficult  or  im- 
possible. When,  for  instance,  a  patient  who  has  had  one  or 
more  attacks  of  rheumatic  fever  and  who  is  distinctly  anaemic, 
is  found  to  be  suffering  from  mitral  regurgitation  presenting 
the  usual  characters  of  regurgitation  due  to  muscular  incom- 
petence, it  is  difficult  or  impossible  to  be  quite  certain  that 
there  are  no  organic  changes  in  the  valve  segments.  Again, 
in  cases  in  which  the  patient  is  known  to  be  the  subject  of 
chronic  mitral  regurgitation  the  result  of  organic  changes  in 
the  valve  segments,  and  is  at  the  same  time  markedly  anaemic, 
it  may  be  difficult  or  impossible  to  decide  what  proportion  of 

'  It  is  important  to  remember  that  in  some  cases  of  this  description  (typhoid, 
typhus,  etc. ),  shortness  of  breath  and  cough  may  be  due  to  lung  compHcations, 
independently  of  any  mitral  lesion  ;  and  that  some  swelling  of  the  feet  may  result 
from  simple  debility.  It  is  therefore  necessary,  before  attaching  much  importance 
to  those  symptoms,  to  be  satisfied  that  the  shortness  of  breath  depends  upon 
cardiac  causes,  and  not  upon  (primary)  lung  disease  ;  and  that  the  dropsy  is  con- 
siderable and  progressive. 


452  Diseases  of  the  Heart. 

the  incompetence,  so  to  speak,  is  due  to  the  old  organic  lesion 
of  the  valve  segments,  and  what  proportion  to  the  recent 
anaemic  changes  in  the  cardiac  muscle.  The  majority  of 
cases,  which  come  under  observation,  are  fortunately  more 
simple,  and.  in  them  the  question  can  usually  be  determined 
by  attention  to  the  following  points  : — 

1.  The  general  condition  of  the  patient.  —\n  cases  of 
muscular  incompetence  due  to  anaemic  degeneration  of  the 
cardiac  muscle,  the  general  appearance  of  the  patient  at  once 
attracts  attention.  In  chlorosis  and  progressive  pernicious 
anaemia,  which  are  the  affections  in  which  this  question  of 
diagnosis  chiefly  arises,  the  extreme  pallor  of  the  mucous 
membranes,  the  lemon  yellow  colour  of  the  skin,  the  fact  that 
there  is  no  emaciation  so  far  as  the  subcutaneous  fat  is  con- 
cerned, and  the  naked  eye  and  microscopical  characters  of  the 
blood,  are  very  striking  features,  and  show  that  a  distinct 
cause  of  cardiac  muscular  degeneration  is  present.^ 

2.  The  condition  of  the  heart  and  pulse,  as  determined  by 
physical  examination.—  A  mitral  murmur  due  to  muscular 
incompetence,  the  result  of  anaemia,  is  usually  preceded,  and, 
I  believe,  almost  always  accompanied  by  a  basic  systolic 
murmur, — a  pulmonary  systolic  murmur,  or,  more  rarely,  an 
aortic  s}-stolic  murmur,  or  both.  It  is  also  accompanied  by  a 
venous  hum  in  the  neck. 

Palpation  and  percussion  show  that  the  heart  is  dilated 
rather  than  hypertrophicd.- 

There  is  marked  irritability  of  the  cardiac  muscle,  the 
effect  of  which  is  seen  in  the  sharp  and  easily  excitable 
condition  of  the  cardiac  contractions,  and  by  observing  the 
characters  of  the  pulse.  This  'celerity'  and  irritability  of 
cardiac  action  is  noticeable  during  the  whole  course  of  the 
case  though  it  is  probably  more  marked  in  the  earlier  stages. 

'  As  a  matter  of  practical  experience,  we  know  that  in  cases  of  this  description 
the  cardiac  muscle  is  always  fatty. 

■  I  am  obliged  to  differ  from  those  authorities  who  state  that  the  heart  is  not 
dilated  in  progressive  pernicious  anaemia,  for  in  all  the  fatal  cases  of  that  disease 
which  have  come  under  my  own  observation,  there  was  more  or  less  dilatation  of 
all  the  cardiac  cavities.  The  dilatation  is,  however,  never  so  great,  as  we 
frequently  see  it,  in  fatal  cases  of  organic  disease  of  the  valve  segments. 


'  Diagnosis  of  Mitral  Incompetence.  453 

In  the  earlier  stages  of  anaemia  the  tension  of  the  pulse 
is  increased,  as  Dr  Broadbent  and  others  have  pointed  out. 
Dr  Sansom  ^  very  justly,  I  think,  states  that  in  this  fact 
we  have  an  important  differentiating  mark  between  mitral 
regurgitation,  the  result  of  organic  changes  in  the  valve 
segments,  and  that  due  to  anaemic  degeneration  of  the 
cardiac  muscle.  It  must,  however,  be  remembered  that  in 
the  later  stages  of  progressive  pernicious  anaemia  the  in- 
creased tension  of  the  pulse  may  completely  disappear,  as  is 
well  shown  in  the  following  tracing  taken  from  a  case  of 
progressive  anaemia,  which  died  under  my  own  care. 


Fig.    192. — Pulse  tracing  in  progressive  Pernicious  AHLvmia. 

R.  R — ,  set.  17,  admitted  to  Newcastle-on-Tyne  Infirmary,  2 1st  February 
1878,  and  died,  notwithstanding  the  systematic  administration  of  alrsenic,  on 
April  I2th,  1878.  This  tracing  was  taken  on  March  19th;  the  artery  is  ahnost 
empty  during  diastole. 


3.  The  cJiaracter  of  the  imifinur. — The  sound  characters 
and  extent  of  propagation  of  the  murmur  cannot  be  absolutely 
relied  upon  for  diagnostic  purposes.  It  may  be  stated,  however, 
as  a  general  rule,  that  a  murmur  which  results  from  muscular 
incompetence  is  usually  faint,  and  not  well  conducted  ;  while 
a  murmur  due  to  organic  changes  in  the  valve  segments, 
is,  usually,  in  the  earlier  stages  of  the  case^  {i.e.  while  the  left 
ventricle  is  powerful)  loud  and  well  propagated.  Murmurs 
due  to  muscular  incompetence  are  usually  inaudible  at  the 
inferior  angle  of  the  left  scapula. 

'  Lettsomian  Lectures,  p.  43. 

'^  In  consequence  of  the  feeble  action  of  the  left  ventricle,  degeneration  of  its 
muscular  fibre,  etc.,  an  organic  murmur,  which  in  the  earlier  stages  of  the 
case  was  loud  and  distinctly  heard  at  the  inferior  angle  of  the  left  scapula,  may 
become  soft  and  inaudible  in  the  back. 


454  Diseases  of  the  Heart. 

4.  The  severity  of  the  symptoins. — In  cases  of  anemia, 
symptoms,  due  to  venous  engorgement  of  the  peripheral  organs 
and  tissues,  are  much  less  prominent  than  in  cases  of  organic 
disease  of  the  valve  segments  in  which  there  is  the  same 
amount  of  cardiac  degeneration  and  dilatation. 

5.  The  effects  of  treatment. — Chlorosis  and  other  forms  of 
simple  anaemia  can  be  speedily  cured  and  the  heart  restored 
to  its  normal  condition  by  the  use  of  iron  and  other  suitable 
remedies.  In  many  cases  of  pernicious  anaemia  a  perfect  cure 
follows  the  systematic  administration  of  arsenic.  Whereas 
in  mitral  regurgitation  due  to  organic  lesions  of  the  valve 
segments,  although  the  symptoms  may  in  most  cases  be 
relieved  by  appropriate  treatment,  the  mitral  regurgitation, 
and  therefore  the  murmur,  always  remains  ;  in  fact,  with  the 
relief  of  the  symptoms  the  murmur  frequently  becomes 
louder  and  better  marked  in  consequence  of  the  increased 
strength  which  the  ventricular  muscle  acquires  as  the  result 
of  treatment. 

6.  The  history  of  the  case.  —A  history  of  acute  rheumatism 
would,  in  a  doubtful  case,  be  in  favour  of  organic  diseases 
of  the  valve  segments  rather  than  of  muscular  incompe- 
tence. Too  much  weight  must  not,  however,  be  given  to 
this  fact. 

In  cases  of  exophthahnic goitre  the  same  difficulty  in  diag- 
nosis also  occurs.  A  systolic  mitral  murmur  in  this  affection 
is  generally  due  to  the  muscular  or  relative  incompetence 
rather  than  organic  disease  of  the  valve  segments.  Each 
case  must,  however,  be  judged  on  its  own  merits,  in  accord- 
ance with  the  general  principles  just  laid  down. 

In  cases  of  aortic  regiwgitation  it  may  also  be  difficult 
or  impossible  to  say  whether  a  mitral  systolic  murmur, 
which  develops  in  the  later  stages  of  the  disease,  is  due  to 
muscular  and  relative  incompetence,  or  to  organic  changes 
in  the  valve  segments  ;  in  most  cases  it  is,  I  believe,  caused 
by  the  former  condition  (muscular  or  relative  incompe- 
tence). This  point  is  not  one  of  much  practical  importance, 
for    aortic    regurgitation    complicated    with    either    form    of 


Prognosis  of  Mitral  Incompetence.  455 

mitral  incompetence   is  an   extremely  serious  and  incurable 
affection. 

Step  No.  3. —  TJie  regurgitation  is  due  to  muscutar  or  rela- 
tive incompetence ;  is  t/ie  condition  curabte  or  not? 

Step  No.  4. —  7 lie  regurgitation  is  due  to  organic  cJianges  in 
t/ie  valve  segments ;  wliat  is  tJie  extent  atid  gravity  of  tlie 
lesion  ? 

Both  of  these  questions  (Steps  4  and  5)  are  intimately 
connected  with  the  prognosis,  which  I  will  therefore  now 
consider. 

Prognosis.  —  In  considering  the  prognosis  of  mitral  re- 
gurgitation, it  is  essential  to  draw  a  line  of  distinction 
between  cases  of  muscular  and  relative  incompetence  on  the 
one  hand,  and  incompetence  due  to  organic  changes  in  the 
valve  segments,  on  the  other.  The  former  condition  is 
often  completely  curable  ;  the  latter  cannot  be  removed  by 
any  therapeutic  measures  with  which  we  are  at  present 
acquainted. 

The  prognosis  of  mitral  regurgitation  produced  by  mus- 
cular and  relative  incompetence.  Having  decided  that  the 
case  is  one  of  muscular  or  relative  incompetence,  we 
must  next  endeavour  to  determine  whether  the  condition 
is  curable  or  not.  The  point  is  obviously  one  of  the 
greatest  practical  importance,  and  in  many  cases  it  can 
be  determined  with  considerable  certainty.  The  whole 
question  turns  on  the  nature  of  the  cause  of  the  muscular 
debility ;  the  mitral  regurgitation  itself  is  altogether  secondary 
in  importance.  In  cases  of  this  description,  we  know  as 
a  matter  of  practical  experience,  firstly,  that  if  we  can  cure 
the  muscular  degeneration  the  mitral  incompetence  will  dis- 
appear ;  and  secondly,  that  in  many  cases  the  muscular  de- 
generation can  be  completely  removed  by  treatment,  while 
in  others  it  cannot. 

In  a  case  of  mitral  regurgitation  due  to  anaemic  changes 
in  the  cardiac  muscle,  for  example,  we   must  endeavour  to 


456  Diseases  of  the  Heart. 

determine  what  is  the  cause  of  the  anjemia.  If  we  come  to 
the  conclusion  that  the  case  is  one  of  ordinary  chlorosis,  we 
can  with  great  certainty  predict  that  the  condition  will  be 
speedily  and  completely  cured.  If,  on  the  other  hand,  we 
decide  that  the  case  is  one  of  progressive  pernicious  anaemia, 
we  know  that  in  some  cases  the  termination  will  be  fatal.  In 
cases  of  progressive  anaemia  we  can  only,  as  I  shall  afterwards 
point  out,  judge  of  the  curability  of  the  case  by  watching  the 
therapeutic  results.^ 

It  is  quite  impossible  to  consider  here  in  detail  the 
prognosis  of  the  many  different  primary-  conditions  (such  as 
the  acute  febrile  affections,  the  different  forms  of  anaemia, 
exophthalmic  goitre,  etc.),  which  may  be  attended  with 
relaxation  and  degeneration  of  the  cardiac  muscle,  and 
therefore  with  muscular  and  relative  incompetence  of  the 
mitral  orifice.  The  prognosis  of  some  of  these  conditions, 
more  particularly  those  in  which  the  muscular  degeneration  is 
confined  to  the  walls  of  the  heart,  will  be  again  referred  to 
when  treating  of  the  diseases  of  the  myocardium.  The  points 
I  wish  to  emphasise  now  are  that,  the  mitral  incompetence  is 
in  cases  of  this  description  of  secondary  importance,  and  that 
the  object  of  the  physician  must  be  to  ascertain  the  exact 
cause  of  the  muscular  debility  or  degeneration.  It  is  only 
after  this  point  is  ascertained  that  a  rational  and  scientific 
prognosis  can  be  given. 

The  prognosis  of  mitral  reguj'gitation  due  to  organic 
changes  in  the  valve  segments. — Having  come  to  the  con- 
clusion that  the  regurgitation  is  due  to  organic  changes 
in  the  valve  segments,  we  must  next  endeavour  to  de- 
termine what  is  the  gravity  of  the  lesion,  and  in  trying  to 
solve  this  question  it  is  important  to  remember  that  the 
extent  and  the  gravity  of  the  lesion  are  by  no  means 
synonymous  terms.     It  is  only,  when  other  things  (such,  for 

•  I  say  with  considerable  certainty,  for  it  is,  I  believe,  sometimes  impossible  to 
distinguish  cases  of  chlorosis  and  of  progressive  pernicious  anaemia,  except  by 
the  therapeutic  method.  Cases  of  ordinary  chlorosis  are  speedily  cured  by  the 
preparations  of  iron  (such  as  Blaud's  pills),  which  are  quite  useless,  and  indeed 
oftan  do  harm  in  the  '  idiopathic '  form  of  the  disease. 


Prognosis  of  Mitral  hicojupetcnce,  457 

instance,  as  the  general  vitality  and  resisting  powers  of  the 
patient)  are  equal,  that  the  severity  of  the  case  varies  directly 
with  the  amount  of  the  regurgitation. 

In  judging  of  the  gravity  of  the  case,  we  have  therefore  to 
take  into  consideration  the  following  points  : — 

1.  The  amount  of  the  regurgitation. 

2.  The  capabilities  of  compensation,  and  the  powers  of 
resistance  possessed  by  the  particular  patient  under  observa- 
tion. 

3.  Whether  the  lesion  of  the  mitral  valve  is  progressive  or 
stationary. 

4.  The  presence  or  absence  of  complications. 
Let  us  consider  each  of  these  points  in  detail. 

The  amount  of  the  regurgitation. — The  mere  characters  of 
the  murmur  give  us  no  information  as  to  the  amount  of  the 
regurgitation.  It  is  important  to  direct  attention  particularly 
to  this  point,  for  it  is  sometimes  supposed  that  a  loud  murmur, 
which  is  well  propagated,  is  indicative  of  more  serious  disease 
than  a  soft,  localised  bruit.  In  many  cases,  the  reverse  is  the 
fact ;  indeed,  we  often  find,  as  I  have  previously  pointed  out, 
that  a  murmur  which,  in  the  earlier  stages  of  the  case,  was 
loud  and  well  propagated,  may,  with  the  appearance  of  grave 
symptoms,  become  soft  and  faint,  or  disappear  altogether  ;  the 
increased  severity  of  symptoms,  and  the  diminished  loudness 
of  the  murmur,  both  being  due  to  failure  of  the  muscular 
power  of  the  heart. 

In  order  to  form  an  opinion  as  to  the  amount  of  the  re- 
gurgitation, we  must  take  into  account : — 

Firstly,  the  extent  of  the  secondary  changes  produced  in 
the  heart  itself;  and  secondly,  the  amount  of  mechanical  de- 
rangement produced  in  the  arterial  and  venous  circulations 
respectively. 

The  degree  of  accentuation  of  the  pulmonary  second  sound, 
the  amount  of  the  secondary  hypertrophy  and  dilatation  of  the 
right  heart,  and  the  severity  of  the  lung  symptoms,  are  the 
points  to  which  attention  is  to  be  directed  in  judging  of  the 
severity  of  the  pulmonary  congestion. 


458  Diseases  of  the  Heart. 

The  condition  of  the  systemic  venous  system,  as  determined 
by  physical  examination,  the  extent  of  the  dropsy  and  of  the 
other  secondary  effects  of  systemic  venous  engorgement,  enable 
us  to  determine  the  extent  of  the  obstruction  to  the  venous 
return  through  the  systemic  veins. 

The  condition  of  the  radial  pulse,  more  particularly  when 
compared  with  the  size  and  strength  of  the  left  ventricle,  gives 
information  as  to  the  extent  of  interference  with  the  arterial 
circulation. 

TJie  paticnfs  capability  of  resisting  the  disease. — The 
patient's  power  of  bearing  up  under  the  lesion  and  resisting 
its  bad  effects  depends  upon  : — 

1.  The  power  of  compensation  or  resistance  possessed  by 
the  heart  itself 

2.  The  power  of  resistance  possessed  by  the  other  tissues 
and  organs. 

3.  His  circumstances,  habits,  and  surroundings. 

I.  The  capabilities  of  compensation  or  resistance  possessed  by 
the  heart  itself. — We  have  previously  seen,  that  compensation 
is  for  the  most  part  effected  by  the  production  of  secondary 
hypertrophy  of  the  walls  of  the  heart.  (See  p.  55.)  Now,  for 
the  production  of  satisfactory  hypertrophy,  several  conditions 
are  necessary.  In  the  first  place,  the  muscular  tissue  of  the 
heart  must  be  healthy  ;  when  it  is  diseased,  when,  for  instance, 
it  is  in  a  condition  of  fatty  or  fibroid  degeneration,  the  hyper- 
trophy is  never  very  satisfactory.  In  the  second  place,  the 
muscle  must  receive  a  sufficient  supply  of  healthy  arterial 
blood.  In  the  tJdrd  place,  the  waste  products  of  its  combus- 
tion must  be  quickly  removed ;  and,  in  the  foiirtJi  place,  its 
trophic  nerve  apparatus  must  be  healthy. 

In  endeavouring  to  ascertain  tJie  condition  of  the  cardiac 
muscle,  it  is  well  to  remember,  that  in  chronic  cases  of  mitral 
regurgitation,  the  lesion  has  generally  been  slowly  and  gra- 
dually progressing  for  months,  it  may  be  for  years,  before  the 
patient  comes  under  observation  ;  and  that  it  is  usually  the 
failure  of  the  compensation,  which  produces  the  symptoms  anu 


Prognosis  of  Mitral  Incompetence.  459 

which  causes  the  patient  to  consult  a  physician.  Now,  in  cases 
of  this  description,  we  are  guided  to  a  considerable  extent  in 
forming  an  opinion  as  to  the  condition  of  the  cardiac  muscle 
by  the  physical  examination  of  the  heart  {i.e.  by  the  size  of  the 
heart  and  of  its  different  cavities,  the  character  of  its  impulse), 
and  by  observing  the  condition  of  the  venous  and  arterial 
systems.  The  following  points  must  also  be  taken  into  con- 
sideration : — 

{a)  The  age  of  the  patient. — In  youth  the  cardiac  muscle 
is  generally  healthier,  and  the  capabilities  of  repair  are  greater, 
than  at  more  advanced  periods  of  life. 

{b)  T/ie  atiology  of  tlie  case. — When  the  regurgitation  has 
resulted  from  acute  endocarditis,  the  capabilities  of  repair  are 
generally  greater  than  when  it  is  due  to  atheroma  or  other 
degenerative  changes.  There  are,  however,  many  exceptions 
to  this  rule.  An  organic  valvular  lesion  due  to  acute  endo- 
carditis is  more  frequently  complicated,  for  example,  with  an 
adherent  pericardium,  the  result  of  pericarditis,  or  with  degene- 
ration of  the  muscular  wall  of  the  heart,  the  result  of  endo- 
carditis, than  an  organic  valvular  lesion  due  to  other  causes  ; 
and  these  complications  (adherent  pericardium  and  fibroid 
degeneration,  the  result  of  myocarditis)  add  most  materially  to 
the  gravity  of  the  case. 

(c)  TJie  facility  with  ivhich  the  cardiac  muscle  responds  to 
the  administration  of  cardiac  toftics,  such  as  digitalis. — This  is 
a  point  of  great  practical  importance,  for  by  administering 
cardiac  tonics,  and  by  watching  their  effects,  we  have  an  im- 
portant means  of  ascertaining  the  condition  of  the  cardiac 
muscle.  In  cases  of  fatty  and  fibroid  degeneration,  for  ex- 
ample, the  administration  of  digitalis  often  produces  no  bene- 
ficial effect. 

In  trying  to  ascertain  zvhether  a  sufficient  amount  of  healthy 
blood  is  supplied  to  the  cardiac  muscle  we  must  observe  : — 

{a)  The  condition  of  the  organs  concerned  in  the  manufac- 
ture and  aeration  of  the  blood,  and  in  the  separation  from  it  of 
waste  products,  more  particularly  the  condition  of  the  stomach, 
liver,  and  kidneys. 

{]))  The  effect  of  the  lesion  on  the  arterial  system.     If  the 


460  Diseases  of  the  Heart. 

radial  pulse  is  very  weak  and  small,  in  consequence  of  the 
mitral  disease,  the  strong  probability  is,  that  the  circulation  in 
the  coronary  arteries  will  also  be  extremely  feeble. 

(r)  The  condition  of  the  coronary  arteries.  We  have  no 
direct  means  of  ascertaining  the  condition  of  the  coronary 
arteries.  Atheroma  of  the  superficial  arteries,  a  dilated  con- 
dition of  the  aortic  arch,  with  or  without  disease  of  the  aortic 
valves,  an  arcus  senilis,  and  pains  of  an  angina-like  character 
are  suggestive  of  atheroma  of  the  coronary  arteries  ;  and 
when  the  coronary  arteries  are  diseased,  the  supply  of  arterial 
blood  to  the  cardiac  muscle  is,  of  course,  still  further  interfered 
with. 

TJie  removal  of  the  zvaste  products  of  tissue  chmigc  from 
the  heart  itself  is,  of  course,  effected  by  the  cardiac  veins. 
When  the  return  current  through  the  cardiac  veins  is  obstructed, 
the  healthy  nutrition  of  the  cardiac  walls  must  to  some  extent 
be  interfered  with.  When  therefore  engorgement  of  the  right 
heart  and  congestion  of  the  systemic  venous  circulation,  which 
are  suggestive  of  impeded  return  through  the  cardiac  veins, 
are  present,  the  prospects  of  satisfactory  hypertrophy  are,  for 
this  and  other  reasons,^  not  very  hopeful.  (It  must,  of  course, 
be  remembered,  that  temporary  engorgement  of  the  right 
heart  and  venous  circulation,  the  result  of  intercurrent  pul- 
monary complications,  such  as  acute  bronchitis,  is  of  frequent 
occurrence  in  the  course  of  mitral  disease.) 

The  condition  of  the  trophic  nerve  apparatus  connected  zvith 
the  heart  probably  has  a  very  important  influence  in  the  pro- 
duction of  satisfactory  hypertrophy.  The  exact  nature  of 
this  mechanism  is  not  yet  understood,  though  Dr  Gaskell's 
researches  seem  to  show,  as  I  have  previously  pointed  out 
(see  page  33),  that  the  vagus  exerts  some  sort  of  trophic 
influence  upon  the  cardiac  muscle.  Be  that  as  it  may,  a 
healthy  condition  of  the  nervous  system,  and  a  serene  placid 
and  happy  disposition  exert  a  most  important  influence  on  the 
course  of  all  cardiac  cases,  and  undoubtedly  aid  in  the  produc- 
tion of  satisfactory  compensation. 

•  An  engorged  condition  of  the  right  heart  and  of  the  systemic  venous  circula- 
tion are  indicative  of  an  advanced  mitral  lesion. 


Pi'ogiwsis  of  Mit7'al  Incompetence.  461 

2.  Tlie  poiver  of  resistance  possessed  by  the  peripJiei'al  tissues 
and  organs. — Here,  as  in  the  heart,  the  capability  of  resisting 
and  bearing  up  against  the  effects  of  the  lesion  depend  upon  : 
(i)  the  condition  of  the  tissue  itself;  (2)  the  proper  supply  of 
nutrient  material ;  (3)  the  adequate  removal  of  waste  products ; 
and  (4)  the  condition  of  its  nerve  supply. 

The  presence  of  complications,  therefore,  more  especially 
of  diseased  conditions  of  the  stomach  and  other  organs  which 
manufacture  the  nutrient  fluid  ;  of  the  kidneys  and  other  organs 
which  purify  it ;  and  of  the  nervous  system  which  exerts  such 
a  powerful  influence  on  all  the  processes  of  nutrition  and  resist- 
ance, are  most  important  factors  in  determining  the  prognosis 
in  cases  of  mitral  regurgitation. 

3.  The  patients  circumstances,  habits,  and  snrrotindings  also 
exercise  an  important  influence  on  the  progress  of  the  case. 
— Patients  who  are  obliged  to  follow  laborious  occupations, 
who  are  worried  by  financial  or  other  matters,  who  are  badly 
housed,  badly  fed,  and  badly  clothed,  who  are  unable  to  obtain 
medical  advice,  or  who  will  not  or  cannot  carry  out  the  direc- 
tions of  their  medical  attendant,  who  are  exposed  to  the  vicis- 
situdes of  the  weather,  and  who  are  given  to  excesses  of  any 
kind,  succumb  to  a  mitral  lesion  much  more  quickly  than 
others  who  are  more  favourably  situated.  In  them  the  lesion 
progresses  more  quickly,  the  capabilities  of  resistance  are  not 
so  great,  compensation  more  quickly  fails,  and  complications 
on  the  part  of  the  respiratory  organs,  for  example,  are  much 
more  apt  to  arise. 

4.  The  progressive  or  stationary  character  of  the  lesion. 
This  is  an  extremely  important  point,  and  is  determined 

by:- 

{a)  The  history  of  the  case. 

(b)  Close  observation  of  the  case  and  noting  the  condition 
of  the  patient  from  time  to  time. 

(c)  By  comparing  the  duration  of  the  case  and  the  effects 
which  the  lesion  has  already  produced  on  the  heart  and  circu- 
lation— the  progress  of  the  symptoms,  etc. 

{d)  The  nature  of  the  morbid  process  ;  mitral  regurgitation 


462  Diseases  of  the  Heart. 

caused  by  atheroma,  for  instance,  will  be  more  likely  to  progress 
rapidly  than  incompetence  due  to  endocarditis.  It  is  difficult, 
however,  to  lay  down  any  general  rule  on  this  point. 

The  associated  pathological  conditions. — The  important  in- 
fluence which  complications  exercise  upon  the  course  of  mitral 
regurgitation  has  already  been  pointed  out  in  speaking  of  the 
patient's  power  of  resistance,  and  need  not,  therefore,  be  again 
referred  to. 

The  advisability  of  communicating  to  or  ivithholding  from  the 
the  patient  the  knowledge  that  the  heart  is  diseased,  is  a  question 
which  always  requires  careful  consideration.  In  most  cases,  it 
is,  in  my  opinion,  highly  desirable  to  deal  frankly,  though  of 
course  the  very  reverse  of  abruptly,  with  the  patient  ;  for  unless 
he  realises  the  fact,  that  his  heart  is  organically  diseased,  he 
cannot  intelligently  carry  out  our  instructions  as  to  treatment, 
and  he  does  not  guard  himself  so  carefully,  as  he  otherwise 
would  do,  against  many  things,  such  as  over-exertion,  exposure 
to  cold,  etc.,  which  aggravate  the  disease  or  induce  complica- 
tions. In  some  cases,  the  communication  should  be  made  in 
a  very  guarded  manner;  and  in  the  case  of  very  nervous  and 
easily  depressed  people,  it  is  occasionally,  though  rarely,  desir- 
able to  withhold  the  information  altogether.  In  cases  of  this 
description,  the  physician  should  take  care  to  protect  himself 
against  accidents,  by  communicating  the  exact  condition  of 
the  patient  to  some  judicious  relative,  for  should  this  commu- 
nication not  be  made,  and  the  fact  that  the  heart  is  affected 
be  subsequently  discovered  (by  some  other  physician,  for  ex- 
ample, or  by  the  death  of  the  patient),  it  may  be  supposed 
that  the  cardiac  lesion  was  not  recognised.  In  all  cases  of 
mitral  regurgitation  in  which  the  patient  is  informed  of  his 
condition,  he  should  be  impressed  with  the  fact  that  the  lesion 
has  little  or  no  tendency  to  result  in  sudden  death. 

Treatment.  —  The  first  indicatioJi  for  the  treatment  of 
mitral  regurgitation,  and  indeed  of  all  diseases,  is  to  effect  a 
cure  by  removing  the  cause  of  the  disease. 


Treatment  of  Mitral  Regurgitation.  463 

When  the  regurgitation  is  due  to  '  muscular '  and  '  relative  ' 
incompetence,  the  debilitated  or  degenerated  condition  of  the 
cardiac  muscle,  on  which  the  regurgitation  depends,  can  often 
be  completely  cured ;  when  the  incompetence  is  due  to  organic 
changes  in  the  valve  segments,  this  happy  result  cannot  be 
attained,  for  we  know  of  no  therapeutic  measures  by  which  a 
sclerosed  valve  can  be  restored  to  its  previous  healthy  condi- 
tion. It  is  necessary,  therefore,  to  describe  separately,  the 
treatment  appropriate  to  each  of  the  two  forms. 

The  treatment  of  mitral  regurgitation  due  to  muscular  and 
relative  incompetence. 

The  incompetence,  which  is  due  to  febrile  changes  in  the 
cardiac  muscle,  almost  invariably  disappears  during  the  course 
of  convalescence,  and  does  not  call  for  any  special  treatment. 
The  main  indication  is  to  restore  the  tone  of  the  general 
health  by  suitable  food,  fresh  air  and  general  tonics,  amongst 
which  iron,  quinine,  and  strychnine  are  most  useful.  In  the 
earlier  stages  of  convalescence,  when  the  cardiac  degeneration 
is  most  marked,  the  patient  should  be  cautioned  against  sud- 
den effort,  such  as  quickly  rising  from  the  recumbent  to  the 
standing  position,  and  against  everything  which  is  likely  to 
increase  the  cardiac  weakness,  or  to  induce  syncope  ;  prolonged 
immersion  in  a  warm  bath,  for  example,  is  to  be  avoided — 
I  have  known  alarming  indications  of  cardiac  failure  produced 
by  a  Turkish  bath  in  a  patient  convalescent  from  rheumatic 
fever — tobacco  smoking  should  be  very  sparingly,  if  at  all, 
indulged  in,  and  sexual  intercourse  altogether  avoided.  These 
points  are,  however,  so  obvious,  that  I  need  not  go  into 
details. 

When  the  incompetence  is  due  to  fatty  changes  in  the 
cardiac  muscle,  the  pathological  change  on  which  the  fatty 
condition  of  the  cardiac  muscle  depends  must  be  combated. 

In  chlorosis  and  all  the  ordinary  forms  of  anaemia,  iron  or  a 
combination  of  iron  and  arsenic,  arc  the  most  useful  drugs. 
The  diet  should  be  light  and  nutritious  ;  the  patient  should 
have  plenty  of  fresh  air  and  outdoor  exercise.  The  ventila- 
tion of  the  sitting  and  sleeping  rooms  must  be  particularly 


464  Diseases  of  the  Heart. 

attended  to.  Any  exhausting  discharge  must,  of  course,  at 
the  outset,  be  arrested.^ 

In  cases  of  pernicious  anaemia  iron  is  not  only  useless,  but 
in  some  cases  seems  actually  injurious.  The  systematic  ad- 
ministration of  arsenic — beginning  with  two  or  three  drops, 
and  gradually  increasing  the  dose — is  the  only  drug  treatment 
which,  in  my  experience,  is  likely  to  be  attended  with  satis- 
factory results.  Many  cures,  of  undoubted  cases  of  this  (pre- 
viously) intractable  disease,  have  been  published,  since  I  first 
recommended  the  use  of  this  drug  in  the  year  1877.  It  is  not, 
however,  invariably  successful.  I  myself  have  met  with  cases 
in  which  it  has  failed,  and  other  observers  have  recorded  the 
same  experience.  It  is  most  successful  when  given  early  in  the 
disease,  and  it  must  be  persevering/}'  administered  in  gradually 
increasing  doses.  I  know  of  no  means  by  which  we  can 
distinguish  the  cases  of  progressive  anaemia  which  are  curable 
by  arsenic  from  the  cases  which  resist  this  plan  of  treatment. 
We  can  only,  in  fact,  form  a  judgment  of  the  probable  effects 
of  the  treatment  by  observing  the  results.  In  addition  to  the 
administration  of  arsenic,  the  dietetic  and  general  management 
of  the  case  must  be  carefully  attended  to  ;  but  space  will  not 
allow  me  to  enter  into  details  with  regard  to  the  treatment  of 
this  and  other  special  forms  of  disease  (such  as  leucocytha^mia, 
Addison's  disease,  etc.),  in  which  anaemia  is  a  prominent 
symptom.  I  must  repeat,  that  the  mitral  incompetence,  is  in 
these  cases,  a  point  of  altogether  secondary  importance,  and 
does  not  call  for  any  special  plan  of  treatment.  All  our 
therapeutic  measures  must  be  devoted  to  the  primary  condi- 
tion on  which  the  debilitated  and  degenerated  condition  of  the 
cardiac  muscle  depends. 

In  cases  of  exophthalmic  goitre,  muscular  incompetence  at 
the  mitral  orifice  sometimes  also  occurs.  Iron  combined  with 
digitalis,  and  arsenic  are  the  drugs  which  I  have  found  most 
useful  in  this  affection.     It  is  seldom,  however,  that  they  effect 

•  In  cases  of  chlorosis,  iron  is  best  administered  in  the  form  of  Blaud's  pills, 
the  tincture  of  the  muriate,  or  the  saccharine  carbonate.  Arsenic,  in  the  form  of 
Fowler's  solution,  may  be  given  in  combination  with  iron  wine  (Vinum  ferri)  or 
with  the  tincture  of  the  muriate. 


Treatment  of  Mitral  Incompetence.  465 

a  cure.  Dr  Sansom^  has  found  great  improvement  follow  gal- 
vanisation of  the  cervical  sympathetic.  He  uses  twenty  to 
forty  Leclanche  elements,  one  pole  being  placed  behind  the 
lower  jaw  in  front  of  the  sterno-mastoid,  and  the  other  either 
at  a  corresponding  point  of  the  opposite  side,  or  over  the  ver- 
tebra prominens,  or  above  the  sternum  at  the  inner  edge  of 
the  sterno-mastoid  muscle.  In  these  cases,  and  indeed  in  all 
conditions  in  which  the  cardiac  muscle  is  debilitated  and 
degenerated,  the  application  of  a  galvanic  or  Faradic  current 
to  the  vagus  is  likely,  I  think,  to  prove  useful.  The  experience 
which  I  have  had  in  this  method  of  treatment  does  not  as 
yet  allow  me  to  speak  positively  on  the  subject.  I  base  the 
treatment  on  the  opinion  of  Gaskell,  that  the  vagus  exerts  a 
trophic  influence  on  the  heart.^ 

When  the  incompetence  is  associated  with,  or  depends 
upon,  increased  tension  in  the  systemic  arterial  system,  one  of 
the  most  important  indications  is  to  reduce  the  general  blood 
pressure.  In  cases  of  this  description  alcohol  must  be 
absolutely  forbidden,  butcher  meat  must  be  taken  very 
sparingly,  purgatives  must  be  periodically  administered 
(according  to  Dr  Broadbent  a  calomel  pill  is  the  best  pur- 
gative for  this  purpose)  and  alkalis,  such  as  bicarbonate  and 
nitrate  of  potash,  prescribed  ;  iodide  of  potassium  and  chloral 
are  often  useful. 

The  treatment  of  mitral  regurgitation  due  to  organic  changes 
in  the  valve  segments  and  tcndijious  cords. — In  considering  the 
treatment  of  mitral  regurgitation  due  to  organic  changes  in 
the  valve  segments  or  tendinous  cords  it  is  important  to 
remember  :— 

(i)  That  the  chronic  and  sclerotic  lesions  of  the  valve 
segments  cannot  be  removed  by  any  method  of  treatment 
with  which  we  are  at  present  acquainted  ;  and  that  our  treat- 
ment must,  therefore,  be  directed  to  maintaining  the  balance 
of  compensation  and  enabling  nature  to  remedy  and  resist  the 
defect. 

(2)  That  in  some  cases  the  lesion  is  completely  stationary, 

'  Lettsomian  Lectures,  p.  46.  ^  See  p.  33. 

G  G 


466  Diseases  of  iJie  Heart. 

and  of  such  slight  extent  that  although  its  presence  is  demon- 
strated by  the  persistence  of  a  systolic  apex  murmur,  it  is  not 
attended  with  an}'  evident  secondary  alterations  in  the  heart 
itself,  nor  with  any  mechanical  derangement  of  the  circulation. 
In  cases  of  this  description,  in  which  there  are  no  symptoms, 
and  in  which  the  pulmonary  second  sound  may  be  only 
slightly,  if  at  all,  accentuated,  no  special  treatment  is  required. 
The  patient  must  be  directed  to  attend  to  the  condition  of  the 
general  health,  to  avoid  cardiac  strain,  and  exposure  to  cold 
and  other  conditions  likely  to  produce  acute  rheumatism  and 
endocarditis.  The  management  of  these  cases  is  very  similar 
to  that  of  cases  of  progressive  mitral  disease  before  tiic  faihire 
of  compensation. 

(3)  That  in  some  cases  in  which  the  lesion  is  more  serious 
and  is  progressive,  the  compensation  is  for  a  time  so  perfect 
that  there  is  no  mechanical  derangement  of  the  circulation 
and  therefore  there  are  no  symptoms ;  that  in  such  cases  the 
compensation  may  ultimately  fail,  and  all  the  serious  symptoms 
of  venous  engorgement,  which  have  been  previously  detailed, 
result. 

(4)  That  mitral  regurgitation  due  to  organic  changes  in  the 
valve  segments  is  often  associated  with  incompetence  due  to 
defective  muscular  closure  of  the  valvular  orifice  {i.e.  muscular 
and  relative  incompetence),  muscular  incompetence  being 
especially  common  after  the  failure  of  compensation,  when  the 
walls  of  the  left  ventricle  become  degenerated,  and  its  cavity 
dilated.  When  there  is  any  reason  to  suppose  that  the 
ventricular  muscle  is  at  fault,  and  that  muscular  or  relative 
incompetence  is  present,  the  treatment  which  has  been  pre- 
viously recommended  for  those  conditions  must  be  adopted. 
In  all  cases  of  mitral  regurgitation,  for  example,  in  which  the 
patient  is  anaemic — even  when  organic  disease  of  the  valve 
segments  is  known  to  be  present — it  is  a  good  general  rule 
of  practice  to  treat  the  aucxmia  by  the  administration  of 
iron,  arsenic,  and  the  means  to  which  I  have  previously 
referred. 

Bearing  the  general  statements  in  view,  we  may  now  pro- 
ceed to  consider  the  treatment  of  progressive  mitral  disea.se, 


Treatment  of  Mitral  Ineonipetenee.  467 

due  to  organic  changes  in  the  valve  segments,  before  and  after 
the  failure  of  compensation,  respectively. 

The  treatment  of  progressive  viitral  disease  before  tJie  failitre 
of  compensation. — So  long  as  the  compensation  is  perfect,  the 
administration  of  drugs  which  act  directly  upon  the  heart 
itself  is  uncalled  for.  It  must  not,  however,  be  supposed, 
that  in  cases  of  this  description  all  treatment  may  be  dis- 
pensed with  ;  on  the  contrary,  though  drug  treatment  is  seldom 
required,  the  general  management  of  the  patient  must  be  most 
particularly  attended  to.  The  great  objects  which  must  be 
kept  in  view  in  the  treatment  are  : — 

(i)  To  maintain  the  tissues  as  a  whole,  and  the  cardiac 
muscle  in  particular  in  the  highest  state  of  health,  so  as  to 
enable  nature  to  keep  up  those  secondary  changes  which  com- 
pensate the  lesion  and  to  resist  the  evil  effects  of  mechanical 
derangement  of  the  circulation. 

(2)  To  avoid  everything  which  is  likely  to  hasten  the  pro- 
gress of  the  valvular  lesion. 

In  order  to  accomplish  these  objects,  it  is  essential  in  the 
first  place,  to  keep  the  circulation  as  tranquil  as  possible,  and 
to  avoid  everything  which  is  likely  to  throw  any  strain  upon 
the  heart.  If  the  patient  has  been  in  the  habit  of  following  a 
laborious  occupation  he  should  be  advised  to  give  it  up  and 
to  get  some  light,  indoor  employment ;  all  sudden  efforts,  such 
as  lifting  heavy  weights,  hurrying  for  trains,  etc.,  should  be 
strictly  prohibited  ;  gentle  outdoor  exercise  is,  however,  de- 
cidedly beneficial  ;  the  amount  of  exercise  which  is  advisable 
must  be  determined  by  the  special  circumstances  of  each 
individual  case ;  there  is  little  difficulty  in  deciding  this  point, 
for  in  mitral  cases  any  over-exertion  on  the  part  of  the  heart 
at  once  makes  itself  felt  in  the  form  of  shortness  of  breath  ; 
any  exercise  may  be  safely  indulged  in,  which  does  not  cause 
shortness  of  breath,  and  which  does  not  produce  excessive 
fatigue,  vice  versa  every  kind  of  exertion  which  does  produce 
shortness  of  breath  or  excessive  fatigue  should  be  prohibited. 

For  the  same  reasons  everything  which  produces  mental 
worry  and  anxiety  is  to  be  avoided.  The  patient's  surround- 
ings  should   be   as  bright  and  cheerful  as   possible,   and   he 


468  Diseases  of  tJic  Heart. 

should  not  be  allowed  to  take  too  serious  a  view  of  his  own 
condition.  With  this  end  in  view  it  is  generally  advisable  in 
the  case  of  sensible  and  intelligent  patients,  to  explain  clearly 
the  exact  nature  of  the  affection,  the  objects  of  treatment,  the 
accidents  and  complications  which  may  arise,  and  the  manner  in 
which  they  are  to  be  guarded  against.  The  fact  that  the  disease 
has  little  or  no  tendency  to  cause  sudden  death  should  be  im- 
pressed upon  the  patient ;  many  of  the  laity,  when  they  are 
told  that  their  hearts  are  not  quite  sound,  jump  to  the  conclu- 
sion that  they  are  affected  with  a  disease  which  may  at  any 
moment  prove  fatal,  and  to  persons  of  a  nervous  and  anxious 
disposition  this  idea  is  often  a  source  of  perpetual  and  terrible 
anxiety.  It  is  of  the  utmost  importance,  therefore,  to  assure 
the  subjects  of  mitral  regurgitation  that  they  need  have  no 
apprehension  of  sudden  death.  Excesses  of  all  kinds,  more 
especiall}^  o\-cr-indulgence  in  alcohol,  in  tobacco,  or  i)i  venere, 
should  be  strictly  forbidden. 

In  the  second  place,  the  condition  of  the  digestive  and 
excretory  organs  must  be  carefully  attended  to.  The  diet 
should  be  nutritious,  but  easily  assimilated  ;  milk,  farinaceous 
foods,  well-cooked  and  tender  vegetables,  a  small  quantity 
of  butcher  meat,  fish,  poultry,  and  game,  may  be  allowed  ; 
pastry,  rich  made-dishes,  and  too  much  butcher  meat,  are  to 
be  avoided. 

In  those  cases  in  which  there  is  a  tendency  to  excessive 
fat  formation,  the  amount  of  saccharine,  starchy  and  fatty 
articles  of  food  should  be  restricted.  It  is  difficult  to  lay  down 
precise  rules  as  to  the  amount  of  each  article  which  may  be 
allowed,  for  in  each  case  the  needs  of  the  individual  organism 
must  be  taken  into  account.  It  is  important,  however,  to 
remember  that  most  persons,  if  left  to  themselves,  err  on  the 
side  of  excess,  and  that  affectionate  and  well-meaning  relatives 
are  very  apt,  through  mistaken  kindness,  to  do  harm  by  over- 
feeding patients. 

Alcohol  is  not  necessary  in  this  stage  of  the  disease  ;  per- 
sons who  have  been  accustomed  to  the  use  of  wine  or  other 
alcoholic  stimulants  may  be  allowed  a  small  quantity  of 
alcohol,  but  the  quantity  should  be  strictly  moderate,  a  larger 


Treatment  of  Mitral  Incompetence.  469 

amount  is  not  only  in  itself  hurtful,  but  by  producing  a  toler- 
ance on  the  part  of  the  system,  it  robs  us,  in  the  later  stages 
of  the  disease,  of  one  of  our  most  effective  therapeutic  means 
of  arousing  the  failing  heart  to  greater  activity. 

Over-indulgence  in  tea  and  coffee  must  also  be  prohibited. 
Smokers  may  be  allowed  a  small  quantity  of  mild  tobacco, 
but  the  amount,  as  in  the  case  of  alcohol,  should  be  strictly 
moderate. 

The  condition  of  the  excretory  organs,  the  bowels,  liver, 
kidneys,  and  skin,  must  be  carefully  attended  to. 

An  abundance  of  fresh  air  is  eminently  desirable.  As  has 
been  stated  above,  out-door  exercise,  which  neither  produces 
shortness  of  breath  nor  fatigue,  is  to  be  recommended.  It 
is  of  no  less  (probably  of  still  more)  importance  to  have 
plenty  of  fresh  air  indoors,  the  proper  ventilation  of  the 
sitting  and  sleeping  apartments  is,  in  the  case  of  mitral 
disease  (and  indeed  of  all  diseases),  a  point  of  the  very  first 
importance. 

The  patient  should  be  recommended  to  go  to  bed  early, 
and  to  take  a  large  amount  of  sleep. 

In  the  thii'd  place,  complications  of  all  kinds  must  be 
guarded  against.  It  is  particularly  important  to  avoid  ex- 
posure to  cold  and  wet,  for  the  congested  condition  of  the 
respiratory  organs,  which  is  usually  present  in  cases  of  mitral 
disease,  even  when  the  compensation  is  apparently  perfect, 
predisposes  the  patient  to  attacks  of  bronchial  catarrh  and 
other  pulmonary  affections. 

In  many  cases  of  mitral  disease  there  is  also  a  predisposi- 
tion to  rheumatism — a  complication  which  is,  of  course,  to  be 
specially  dreaded  in  the  case  of  patients  who  are  already  the 
subjects  of  chronic  valvular  lesions. 

The  clothing  must  be  warm,  but  not  too  heav}- ;  the  under- 
clothing, in  particular,  must  be  sufficient ;  flannel  should  be 
worn  next  the  skin. 

TJic  treatment  of  progressive  mitral  disease  after  the  failure 
of  compensation. — The  general  plan  of  treatment  suitable  be- 
fore the  failure  of  compensation  should,  so  far  as  is  possible,  be 


470  Diseases  of  the  Heai't. 

continued,  unless  there  is  any  reason  to  the  contrary,  and  the 
following  additional  indications  are  to  be  carried  out : — 

(i.)  To  strengthen,  and,  when  necessary,  to  stiinnlate  the  fail- 
ing action  of  the  heart  by  the  administration  of  cardiac  tonics 
and  stiniidants. 

Some  of  the  most  important  cardiac  tonics  are  digitalis, 
convallaria  majalis,  caffeine,  casca,  strophanthus,  arsenic,  iron, 
and  strychnine. 

Digitalis  is  especially  valuable  in  mitral  regurgitation,  and 
is,  in  fact,  the  remedy  in  progressive  cases,  such  as  we  are  at 
present  considering.  It  seems  to  act  as  a  true  cardiac  tonic, 
regulating  the  rhythm,  diminishing  the  frequency  of  the  heart- 
beats, and  strengthening  the  contractions  of  the  cardiac 
muscle  ;  while  at  the  same  time  it  exerts  a  tonic  effect  upon 
the  muscular  coat  of  the  minute  arteries,  and  produces  an 
increase  of  the  arterial  blood  pressure.  The  tincture  and  the 
infusion  of  the  fresh  leaves  are  the  most  satisfactory  prepara- 
tions ;  and  in  prescribing  this  powerful  remedy,  we  must  en- 
deavour, as  Professor  Sydney  Ringer  points  out,  '  to  obtain 
the  greatest  therapeutic  effect  with  the  smallest  possible  dose;'^ 
five  to  ten  drops  of  the  tincture,  and  two  to  four  drachms  of 
the  infusion,  three  times  daily  are,  as  a  rule,  amply  sufficient. 
When  it  is  desirable  to  produce  a  more  rapid  effect  (as,  for 
instance,  in  those  cases  in  which,  when  the  patient  first  comes 
under  observation,  the  dropsy  is  already  considerable  or  great, 
the  cyanosis  marked,  the  respiration  much  embarrassed,  the 
urine  scanty  and  loaded  with  lithates,  the  pulse  very  small, 
weak,  and  irregular,  and  the  action  of  the  heart  tumultuous), 
much  larger  doses  may  be  advantageously  given. 

During  a  course  of  digitalis  treatment,  the  effects  of  the 
drug  on  the  pulse,  the  urine,  and  the  dropsy,  must  be  carefully 
watched.  So  long  as  the  urine  remains  scanty  and  deposits 
urates,  full  doses  may  be  safely  continued.  After  free  diuresis 
is  established,  and  more  especially  if  the  pulse  falls  below  70 
the  dose  must  be  immediately  reduced,  or  the  administration 
of  the  drug  suspended  altogether.  In  those  cases  in  which 
digitalis  produces  sickness,  as  it  frequently  does  when  given  in 

'  Handbook  of  Therapeutics,  p.  4S6. 


Treatimut  of  Mitral  Incoinpctcuce.  471 

too  large  quantities,  or  when  too  long  continued,  repeated 
small  doses  of  brandy,  or,  still  better,  in  my  experience,  of 
iced  champagne,  or  a  mixture  of  iced  champagne  and  brandy 
should  be  prescribed. 

Convallaria  majalis.  —  This  remedy  has  of  late  been 
strongly  recommended,  and  seems  to  possess  many  of  the 
beneficial  properties  of  digitalis:  it  increases  the  force  of  the 
cardiac  contractions,  while  it  lessens  the  frequency  of  the 
beats;  at  the  same  time  it  produces  free  diuresis.  It  seems  to 
be  well  borne  ;  it  exerts  no  prejudicial  effect  upon  the  digestive 
organs,  but,  on  the  contrary,  rather  increases  the  appetite  and 
the  action  of  the  bowels.  It  may  be  given  in  the  form  of 
extract  (5-8  grs.  of  Savory  and  Moore's  extract  three  times 
daily),  fluid  extract  (5-20  mms.),  or  tincture  (5-20  drops). 

Caffeine  seems  also  to  be  a  cardiac  tonic,  though  not  nearly 
such  a  powerful  one  as  digitalis.  It  slows  the  action  of  the 
heart,  while  at  the  same  time  it  increases  the  force  of  the 
cardiac  contractions  ;  its  most  powerful  and  useful  effect  in 
cases  of  mitral  regurgitation  is,  however,  its  diuretic  action,  a 
point  to  which  I  shall  frequently  refer  more  in  detail.  Citrate 
of  caffeine  is  a  convenient  preparation,  and  may  be  adminis- 
tered in  3-6  grain  doses  three  times  a  day. 

Casca. — Of  this  drug,  which  has  been  strongly  recom- 
mended by  Dr  Brunton,  I  have  had  no  personal  experience. 

Strophanthus. — This  remedy,  which  has  lately  been  exten- 
sively used  by  Professor  T.  R.  Fraser,  is  a  powerful  cardiac 
tonic,  similar  in  action  to  digitalis,  but  more  energetic.^ 

Arsenic  i?,  a  most  important  cardiac  tonic,  and  should  be 
much  more  frequently  and  systematically  prescribed  in  cases 
of  mitral  regurgitation  than  it  is  at  present.  It  is  especially 
useful  in  those  cases  in  which  the  failure  of  compensation  is 
accompanied  by  fatty  changes  in  the  cardiac  muscle  or  pain 
in  the  region  of  the  heart ;  it  should  be  given  in  the  manner 
already  recommended  in  speaking  of  the  treatment  of  muscular 
and  relative  incompetence.     (See  page  463.) 

Iron,  stryc/inine,  and  quinine,  are  all  most  useful  in  some 

'  Professor  Fraser  intends,  I  believe,  to  publish  before  long  the  results  of  his 
investigations  on  this  drug. 


472  Diseases  of  the  Heart. 

cases  of  mitral  regurgitation,  though  they  can  hardly  be  called 
true  cardiac  tonics  in  the  same  sense  as  digitalis. 

Stimulants. — After  the  failure  of  compensation,  alcoholic 
stimulants,  ether,  spirits  of  chloroform,  carbonate  of  am- 
monia, etc.,  are  often  most  useful,  and  require  to  be  freely 
given.  The  application  of  fly  blisters  to  the  praecordial 
region  is,  also,  in  some  ca.ses  an  effective  means  of  stimulating 
the  flagging  heart. 

It  must  not  be  forgotten  that  the  temporary  administra- 
tion of  cardiac  tonics  and  stimulants  is  often  most  useful  and 
necessary  in  the  earlier  stages  of  the  affection,  i.e.  before 
the  failure  of  compensation  ;  it  is,  in  fact,  impossible  to  draw 
any  hard  and  fast  line  between  the  periods  before  and  after 
compensation  ;  the  remedies  which  are  useful  in  the  one 
stage  are  consequently  often  required  in  the  other ;  even 
when  the  compensation  appears  to  be  perfect,  the  reserve 
force  possessed  by  the  heart  is  very  slight,  and  any  temporary 
condition,  such,  for  example,  as  an  intercurrent  attack  of 
bronchial  catarrh,  which  throws  an  increased  strain  upon  the 
heart,  may  for  the  time  upset  the  balance  and  necessitate  the 
temporary  use  of  cardiac  tonics  and  stimulants. 

(2.)  To  relieve  venous  congestion  and  treat  the  pathologieal 
conditions  and  symptoms  zvhich  result  tJieref'om. 

This  is  a  most  important  indication  in  the  later  stages  of 
mitral  disease.  Space  will  not  permit  me  to  detail  the  special 
means  which  are  required  for  each  individual  complication. 
I  must  content  myself  with  referring  to  some  of  the  more 
important.  And  in  treating  the  venous  engorgement  and  its 
results,  Vv'e  must  never  forget  that  the  mechanical  derange- 
ment of  the  circulation  on  which  they  depend  is  due  to 
defective  action  of  the  cardiac  pump,  and  that  one  most  im- 
portant means  of  treatment  consists  in  the  administration  of 
cardiac  tonics  and  stimulants.  We  may,  then,  lay  it  down  as 
a  general  rule,  that  in  treating  the  bronchial  catarrh,  dropsy, 
dyspepsia,  and  other  conditions  which  result  from  venous 
congestion,  digitalis  or  other  cardiac  tonics  should,  unless 
there  is  good  reason  to  the   contrary,  be  combined  with  the 


Treaivicnt  of  Alitral  Incovipetencc.  473 

drugs  which  are  required  for  the  special  complication  under 
consideration. 

In  addition  to  the  administration  of  cardiac  tonics  and 
stimulants,  we  must  endeavour  : — -firstly,  to  remove  the  venous 
engorgement  by  local  and  general  measures  ;  secondly,  to  im- 
prove the  nutritive  condition  of  the  blood,  by  (a)  careful 
attention  to  the  condition  of  the  chylopoietic  viscera  ;  (b)  by 
promoting  free  action  of  the  stomach,  liver,  intestines,  kidneys, 
and  skin  ;  and  (c)  by  establishing  a  healthier  condition  (tone) 
of  the  nerve  centres. 

I  shall  now  briefly  refer  to  the  special  treatment  of  some 
of  the  more  important  symptoms  which  occur  in  the  latter 
stages  of  mitral  disease  ;  and  for  the  sake  of  convenience,  it 
will  be  well  perhaps  to  commence  at  the  lungs,  and  to  proceed 
backwards  in  the  course  of  the  regurgitant  blood  current, 
rather  than  to  take  the  symptoms  in  the  order  in  which  they 
are  likely  to  arise  in  the  living  patient. 

Lung  complications  and  symptoms. — The  dyspnoea  which  is 
due  to  exertion  does  not  of  course  require  any  other  treatment 
than  rest ;  the  continuous  dyspnoea  and  orthopnoea,  which  are 
often  so  distressing  in  the  later  stages  of  mitral  disease,  are 
best  dealt  with  by  the  administration  of  cardiac  tonics  and 
stimulants,  and  of  remedies  suitable  for  the  lung  complica- 
tions (bronchitis,  oedema  of  the  lungs,  hydrothorax,  etc.)  which 
happen  to  be  present.  If  there  is  much  venous  engorgement, 
the  application  of  dry  cups  over  the  back,  of  leeches  over  the 
praecordia,  or  venesection,  are  in  some  cases  beneficial.  The 
inhalation  of  oxygen  and  compressed  air  is  strongly  recom- 
mended by  some  writers,  and  seems  to  be  useful,  by  counter- 
acting the  highly  venous  condition  of  the  blood. 

Cases  of  continuous  dyspnoea  and  orthopnoea,  in  which 
there  is  often  very  great  general  exhaustion  and  insomnia,  are 
often  most  materially  benefited  by  the  administration  of 
morphia  ;  this  drug,  which  is  best  given  by  subcutaneous  in- 
jection, has  been  highly  recommended  by  Clifford  Allbutt, 
Sansom,  and  others,  and  has  sometimes  proved  most  useful 
in  my  own  hands. 

In    the   exceptional    cases   in  which   a  mitral   lesion   and 


474  Diseases  of  tJic  Heart. 

severe  dyspncea  are  associated  with  high  arterial  tension,  and 
in  some  cases  in  which  Cheyne-Stokes'  respiration  occurs, 
nitrite  of  amyl  should  be  inhaled  during  the  attack  itself; 
nitro-glycerine  in  small  doses  (^  ioth  of  a  grain)  may  be  given 
during  the  intervals  ;  bromide  of  potassium  and  chloral  I  have 
found  most  useful  in  some  cases  of  this  description. 

Bronchitis,  ccdema  of  tJie  lungs,  hydrothorax,  pleiirisy,  pneu- 
monia, and  otlicr  lung  complications. — Space  does  not  permit 
me  to  enter  into  details  with  regard  to  the  treatment  of  the 
complications.  In  all  cases  it  is  advisable  to  combine  cardiac 
tonics,  more  especially  digitalis  and  cardiac  stimulants,  with 
those  remedies  which  the  special  complication  in  each  indi- 
vidual case  demands. 

Hctmoptysis. — The  bleeding  is  seldom  so  profuse  as  to  re- 
quire any  special  treatment ;  in  some  cases  it  seems  rather  to 
give  relief  than  to  be  prejudicial ;  when  the  pulmonary  apoplexy 
is  followed,  as  it  often  is,  with  localised  pleurisy  or  pneumonia, 
the  local  and  general  measures  suitable  for  those  complica- 
tions must  of  course  be  employed. 

Engorgement  of  the  right  heart. — When  cardiac  tonics  and 
stimulants,  purgatives  and  diuretics,  fail  to  relieve  the  engorge- 
ment of  the  right  heart,  the  application  of  a  mustard  poultice 
or  blister  to  the  prsecordial  region  is,  in  some  cases,  beneficial. 
The  most  satisfactory  means  of  relieving  great  engorgement 
of  the  right  heart  is,  however,  the  abstraction  of  blood  by 
leeches  applied  to  the  praecordia,  or  even  by  general  vene- 
section. 

Engorgement  of  the  systemic  ve^ious  circulation. — In  addition 
to  the  free  use  of  cardiac  tonics  and  stimulants,  the  administra- 
tion of  diuretics,  diaphoretics,  and  especially  purgatives  which 
produce  free  watery  evacuations,  are  the  remedies  on  which 
reliance  must  be  chiefly  placed.  Digitalis  and  caffeine  are 
the  most  useful  diuretics,  and  are  advantageously  administered 
in  combination,  as  recommended  by  Brakenridge;^  the  acetate, 

'  Brakenrids^e  thinks  that  cafleine  has  a  direct  action  upon  the  secreting 
structures  of  the  kidney,  and  does  not  produce  its  diuretic  action  as  digitalis  is 
supposed  to  do,  entirely  by  increasing  the  blood  pressure. — [Edinburgh  Medical 
lournal,  August  iSSi,  p.   lOO,  cl  seq.) 


Treatment  of  Mitral  Inconipetenee.  475 

nitrate,  and  bitartrate  of  potash  and  squills  are  also  serviceable. 
I  have  found  nitrite  of  amyl  a  most  valuable  diuretic  in  some 
cases,  more  especially  where  the  arterial  tension  has  been  high, 
and  it  has  been  desirable  to  produce  rapid  distention  of  the 
vessels  of  a  congested  kidney  ;  the  application  of  a  warm 
poultice  or  of  dry  cups  over  the  region  of  the  kidney  is  often 
useful  in  cases  of  this  description.  Jalap,  elaterium,  and 
scammony  are  the  most  useful  purgatives ;  purgatives 
which  are  apt  to  cause  hsemorrhoidal  irritation,  are  to  be 
avoided. 

The  skin  should  be  kept  active  by  washing,  rubbing,  and 
bathing  ;  in  the  later  stages  of  the  disease  it  is  not,  as  a  rule, 
advisable  to  immerse  the  whole  body  in  the  bath,  but  indi- 
vidual portions  should  be  washed  separately.  It  is  important 
to  remember  that  prolonged  immersion  in  a  warm  bath  often 
produces  considerable  depression  ;  patients  with  mitral  disease 
should  therefore  bathe  judiciously. 

Dropsy. — Subcutaneous  dropsy,  which  is  one  of  the 
earliest  indications  of  progressive  mitral  disease,  is  to  be 
treated  : — 

Firstly,  By  the  internal  administration  of  cardiac  tonics 
and  stimulants,  diuretics  and  purgatives. 

Secondly,  By  local  measures.  The  swollen  parts  should, 
if  possible,  be  placed  in  such  a  position  that  the  return 
current  of  blood  to  the  heart  is  facilitated  ;  this  is  easily 
of  course  accomplished  so  long  as  the  dropsy  is  limited  to 
the  lower  extremities.  When  the  dropsy  becomes  great,  it 
may  be  necessary  to  evacuate  the  fluid  either  by  simple 
puncture  or  by  means  of  Southcy's  trocars  ;  whichever  method 
be  adopted  it  is  of  the  greatest  importance  to  remember 
that  erythema  and  low  forms  of  inflammation  are  very  apt 
to  arise  at  the  seat  of  the  punctures,  and  that  this  is  more 
particularly  the  case  when  the  fluids  which  escape  are  allowed 
to  remain  in  contact  with  the  skin  and  to  decompose  ;  the 
greatest  attention  should  be  given  to  cleanliness,  all  sources 
of  external  irritation  avoided,  and  decomposition,  so  far  as 
is  possible  by  antiseptic  means,  prevented. 

Erysipelas  and   gangrene   of  the   skin   which   sometimes 


476  Diseases  of  the  Heart. 

arise,  are  very  serious  complications.  The  local  treatment 
must  of  course  be  conducted  on  general  surgical  principles  ; 
cardiac  tonics  and  stimulants  being  at  the  same  time  freely 
administered. 

(3.)  To  improve  the  quality  of  the  blood  and  attend  to  the 
condition  of  the  ehylopoietic  and  excretory  organs.  It  is  particu- 
larly important  to  attend  to  the  condition  of  the  stomach  ;  it 
must  be  remembered  that  this  organ  shares  in  the  general 
venous  engorgement,  and  that  in  the  later  stages  of  mitral 
disease,  at  all  events,  gastric  catarrh  and  its  resulting  dyspepsia 
are  almost  invariably  present  ;^  the  digestive  powers  of  the 
stomach  arc  consequently  seriously  impaired  ;  the  diet  must, 
therefore,  be  regulated  accordingly.  When  dyspeptic  symp- 
toms are  prominent,  small  quantities  of  easily  digestible  food, 
such  as  milk,  farinaceous  foods,  soups,  raw  eggs  beaten  up  with 
a  little  brandy,  should  be  given  at  frequent  intervals  ;  the 
mineral  acids,  strychnine,  arsenic,  and  infusion  of  calumba  are 
useful  additions  to  the  other  remedies  which  have  been  pre- 
viously recommended.  It  is  sometimes  advisable  to  supple- 
ment feeding  by  the  stomach  by  rectal  alimentation;  enemata 
of  defibrinated  ox-blood  or  the  prepared  peptone  enemata — 
consisting  of  beef,  milk,  and  farinaceous  food — recommended 
by  Dr  Sansom,  are  the  most  suitable  and  convenient  forms  ; 
'  from  two  to  four  ounces  are  injected  slowly  into  the  rectum, 
and  repeated  every  three  or  four  hours. '^  I  cannot  too 
strongly  insist  upon  the  importance  of  careful  regulation  of 
the  diet  in  all  stages  of  progressive  mitral  disease. 

The  action  of  the  liver  must  be  encouraged  by  suitable 
purgative  and  cholagogue  remedies. 

The  importance  of  procuring  free  intestinal  evacuation,  and 
of  attending  to  the  function  of  the  kidneys,  has  already  been 
insisted  upon. 

'  Gastric  catarrh  and  dyspepsia  are  often  also  present  in  the  early  stages. 

-  Dr  Sansom's  Lettsoinian  Lectures,  p.  44.  (The  author  is  speaking  of  the 
treatment  of  cases  of  progressive  pernicious  ana;mia,  but  the  same  means  are  useful 
in  some  cases  of  organic  mitral  disease  in  which  the  functions  of  the  stomach  are 
seriously  impaired.) 


Altiology  of  Mitral  Stenosis.  477 

MITRAL   STENOSIS. 
Definition. — Narrowing-  of  the  mitral  orifice. 

ALtiology.  —Stenosis  of  the  mitral  orifice  is  almost  invari- 
ably due  to  permanent  organic  changes  in  the  segments 
and  base  of  the  mitral  valve  ;  with  rare  exceptions  these 
changes  are  very  slowly  and  gradually  developed.^  It  is 
essentially  a  disease  of  early  life,  and  is,  in  my  experience, 
most  frequently  developed  (it  would  perhaps  be  more  correct 
to  say  most  frequently  detected)  between  the  ages  of  fifteen 
and  twenty-five.  Occasionally,  though  very  exceptionally,  it 
is  congenital,  and  is  then  usually  associated  with  congenital 
tricuspid  stenosis.  In  a  large  proportion  of  cases  it  results 
from  rheumatic  endocarditis,  but  it  would  appear  from  Dr 
Sansom's  obser\^ations  -  that,  unlike  mitral  regurgitation,  it  is 
more  frequently  developed  after  mild  rheumatic  manifestations 
and  in  cases,  in  which  articular  phenomena  were  not  mani- 
fested at  all,  than  after  severe  attacks  of  rheumatic  fever.  Dr 
Sansom's  observations  also  seem  to  show,  that  repeated  attacks 
of  acute  rheumatism  do  not  generally  tend  to  produce  the 
lesion.  Mitral  stenosis  is  much  more  frequent  in  females  than 
in  males,  a  circumstance  which  is  probably  to  be  explained  by 
the  facts  that  the  endocarditis  of  early  life  is  more  likely  to 
result  in  mitral  stenosis  than  the  endocarditis  of  the  fully- 
formed  adult,  and  that  acute  rheumatism  is  three  times  more 
prevalent  in  girls,  between  the  ages  of  eleven  and  fifteen,  than 
it  is  in  boys  at  the  same  age.  It  is  interesting  to  note  that 
chorea  is  also  much  more  frequent  in  girls  than  in  boys. 
There  is  probably,  as  Dr  Barlow  has  suggested,  a  distinct 
relationship  between  the  two  conditions.^ 

Morbid  Anatomy   and  Patliological  Physiotogy.  —  Mitral 

'  Occasionally  narrowing  of  the  mitral  orifice  is  due  to  a  mass  of  vegetations  of 
recent  formation  ;  and  in  very  exceptional  cases  it  has  been  produced  by  the  pres- 
sure of  a  tumour,  the  valve  segments  themselves  being  healthy. 

^  Lctisomiaii  Lectures,  p.  8o. 

^  Two  theories  may  be  advanced  in  order  to  explain  the  greater  liability  of  the 
female  sex  to  chorea  and  mitral  stenosis,  viz.: — (i)  That  the  chorea  and  the  mitral 
stenosis  are  both  the  result  of  rheumatism,  which  is,  as  we  have  seen,  three  times 
more  common  in  girls  between  the  ages  of  eleven  and  fifteen  than  in  boys  at  the 
same  age  ;  and  (2)  that  chorea,  even  when  non-rheumatic,  is  frequently  accom- 
panied by  endocarditis,  which  is  the  cause  of  the  mitral  narrowing. 


4/8  Diseases  of  the  Heart. 

stenosis  is,  as  I   have   mentioned,  almost    invariably  due   to 
permanent  organic  changes.      The  exact   appearances   vary 
somewhat  in    different  cases.      In  some,   the  constriction  is 
chiefly  due  to  the  fact,  that  the  orifice  itself  is  narrowed  by 
sclerotic  and  cicatricial    changes    in    the   fibrous    ring  which 
surrounds  it.     In  cases  of  this  description,  the  orifice,  when 
seen   from   above,  looks  like  a  narrow  slit,^  hence  the  term 
button-hole  mitral  which  has  been  applied  to  it.    (See  fig.  193.) 
The  se"-mcnts  of  the  valve  and  chordjE  are  at  the  same  time 
more  or  less  rigid  and  thickened.       In  other  cases  the  seg- 
ments, chorda;  and  tips  of  the  papillary  muscles  are  all  welded 
to"-ether  into  a  dense  mass  of  cartilagenous-like  tissue,  and 
project  into  the  cavity  of  the  left  ventricle  in  the  form  of  a 
hollow  cone.     A  perfect  cone  of  this  description,  such  as  is 
represented  in  fig.   195   is  rare,  but  in  the  majority  of  cases 
of  mitral  constriction  due  to  endocarditis,  a  tendency  to  this 
formation   is  observed.     These  two  conditions,  narrowing  of 
the  orifice  and  fusion  of  the  segments,  are  generally  associated. 
In  rare  cases,  the  mitral  segments  are  quite  healthy,  and  the 
stenosis  is  due  to  the  presence  of  large  calcareous  nodules  in 
the    muscular  wall    of  the  ventricle.      (See    figs.    196,    197.) 
Deposits  of  this  description  are  usually  associated  with  athero- 
matous degeneration  of  the  arteries  ;   in  some  cases  they  are 
gouty  and  consist  of  urates,  in  others  they  represent,  I  think, 
syphilitic  gummata  which  have  become  calcified.     In  three 
cases  of  this  description,  which  have  come    under  my  own 
observation,  and  in  which  the  valvular  orifice  was  very  notably 
narrowed,  there  were  no  symptoms  or  signs  indicative  of  the 
condition  during  life.     Two  of  the  patients  were  old  people 
who  lived  tranquil  lives  ;  the  third  was  a  man  who  was  for 
some  time  under  my  care,  and  who  died  from  a  large  aneurism 
of  the  descending  thoracic  aorta.     (See  figs.  268  and  269.) 

On  microscopical  examination,  the  thickened  valve  seg- 
ments and  chordae  tendineae  are  found  to  present  the  histo- 
logical characters  of  chronic  endocarditis,  which  have  been 
previously  described. 

'   The  healthy  mitral  valve,  when  seen  from  above,  presents  a  slit-like  appear- 
ance ;  in  stenosis  the  slit  is  narrowed. 


Fig.  193. — Stenosis  of  the  mitral  orijice,  seenfrmn  above.    {Natural  size.) 

Tbe  left  auricle,  which  is  considerably  dilated,  has  been  cut  open  ;  an  ante-mortem 
clot  (6)  fills  the  appendix  and  projects  into  the  cavity  of  the  auricle,  a,  points  to  the 
stenosed  mitral  oriiice;  c,  to  the  closed  foramen  ovale;  of,  to  the  outer  and  posterior 
surface  of  the  left  ventricle. 

Note — In  fig.  195  the  appearance  of  the  valve  as  seen  from  tbe  ventricular  side  is 
shown. 


Fig.  194. 

Interior  of  the  Lefl  Ventrick  showing  (diaphragmatic)  contraction  of  the  Mitral  Valve,  and  digease  of 
the  Aortic  Cusps.  Somewhat  larger  than  the  actual  preparation  (the  ventricle,  at  the  point  of 
origin  of  the  aortic  cusps,  measures  in  the  drawing  3^  in.,  and  in  tlie  actual  preparation  2  J  in.). 

a,  is  situated  on  the  anterior  segment  of  the  mitral  valve ;  the  mitral  cusps,  chordae  tendinea 
and  papillary  muscles  are  welded  together. 

b,  points  to  one  of  the  diseased  aortic  cusps,  it  is  bulged  out  towards  the  ventricle,  its  ventn- 
cular  surface  is  roughened. 

Ci  points  to  a  small,  rough  depression  (ulcer)  on  the  exterior  of  the  aortic  cusp,  b. 


[ANlCuMMlNSbnOsEftl^ 


Pig.  195.    Stenosis  of  the  Mitral  Valve.    (^Natural  size.) 

The  segments  of  the  mitral  valve,  the  chordte  tendineae,  and  the  papillary  muscles  are,  as  it 
were,  fused  together  into  a  dense,  firm  mass.  The  mitral  orifice  is  extremely  contracted,  and 
will  not  admit  the  point  of  the  little  finger.  The  letter  a,  points  to  the  base  of  the  aorta  and 
aortic  valve  flaps ;  b,  anterior  segment  of  mitral  valve ;  c,  c,  thickened  chordae  tendinese  and 
papillary  muscles. 

Note. — The  auricular  surface  of  the  stenosed  valve  is  represented  in  fig.  193. 


M'lAUKiCvKMmGLrxo'ED 


Fig.  19t>. — Heart  in  a  case  of  mitral  stenosis,  in  vihich  the  obstruction  was  due  to  the 
deposit  of  large  calcaremis  masses  in  the  base  of  the  valve  and  adjacent  walls  of  the 
heart.     (^Aafural  size,  seen  from  behind.') 

a,  a,  «,  calcareous  masses  surroundiug  the  mitral  orifice,  ■which  is  seen  from  above  ; 
6,  calcareous  mass  in  the  wall  of  the  left  ventricle. 


PafJioIogy  of  Mil  I'd  I  Stenosis. 


A19 


Fig.  197. — Section  through  the  posterior  walls  of  the  left  auricle  ami  ventricle, 

and  through  the  posterior  segment  of  the  7uitral  valve. 

Stenosis  of  the  orifice  was  produced  by  calcareous  nodules,  one  of  which  (a)  is 

shown  in  the  figure,  in  the  base  of  the  valve  ;    the  mitral  cusps  were  healthy  ; 

b,   transversely  divided    wall   of  the    left   ventricle ;   c,    interior  of  left   auricle  ; 

d,  papillary  muscle,  partly  seen  in  section  ;  e,  posterior  segment  of  mitral  valve. 

The  loss  of  elasticity  in  the  valve  segments,  generally 
renders  the  valve  incompetent.  Mitral  stenosis  then,  in  the 
earlier  stages  at  all  events,  is  usually  accompanied  by  mitral 
regurgitation. 

Pathological  Physiology. — T\\q  first  effect  of  mitral  stenosis 
is  to  interfere  with  the  passage  of  the  blood  from  the  cavity 
of  the  left  auricle  to  that  of  the  left  ventricle.  The  left  auricle 
empties  itself  with  difficulty,  its  systole  is  prolonged,  and  blood 
accumulates  and  stagnates  behind  the  obstruction  ;  the  left 
ventricle  receives  a  smaller  supply  of  blood  than  in  health, 
and  the  arterial  system  is,  in  consequence,  imperfectly  dis- 
tended.    Stenosis,  in  short,  produces  more  or  less  engorgement 


480  Diseases  of  the  Heart. 

behind,  and  more  or  less  anaemia  in  front  of  the  mitral  orifice. 
The  second  effect  is  to  produce  a  series  of  changes  in  the- 
heart  itself,  the  other  parts  of  the  circulation,  and  the  peri- 
pheral organs,  which,  with  the  differences  which  I  shall  pre- 
sently mention,  resemble  the  secondary  effects  produced  by 
mitral  regurgitation.     (See  p.  428.) 

The  extent  of  the  primary  and  secondary  effects  of  mitral 
stenosis  varies  with  : — the  extent  of  the  lesion,  the  degree  of 
compensation,  and  the  resisting  power  of  the  patient,  and  of 
his  individual  tissues.  But  since,  in  treating  of  mitral  regur- 
gitation, I  have  already  considered  in  great  detail  the  nature 
of  these  changes  and  the  general  principles  which  determine 
their  production,  I  need  only  now  refer  to  the  points  of 
difference  between  mitral  stenosis  and  mitral  regurgitation. 

In  the  first  place,  then,  mitral  stenosis  differs  from  mitral 
regurgitation  in  the  fact,  that  the  vascular  engorgement  of  the 
left  auricle,  and  consequently  of  the  pulmonary  circulation,  is 
more  continuous.  In  mitral  regurgitation,  the  engorgement  of 
the  left  auricle  and  pulmonary  circulation  is  suddenly  re- 
lieved by  the  occurrence  of  the  ventricular  diastole  ;  and  the 
blood  which  has  been  pent  up,  so  to  speak,  in  the  cavity  of 
the  left  auricle  and  in  the  lungs,  during  the  ventricular  systole, 
has  no  difficulty  in  passing  onwards  into  the  cavity  of  the  left 
ventricle.  But  in  mitral  stenosis  the  obstruction  persists, 
during  the  ventricular  diastole.  When  the  orifice  is  much 
stenosed  (more  especially  in  the  terminal  periods  of  the  case, 
z>.  after  the  auricle  has  become  dilated  and  its  muscular  wall 
paralysed^),  the  left  auricle  is  never  emptied  ;  clots  are 
extremely  apt  to  form  in  the  appendix  (see  figs.  193  and 
198),  and   even   in  the  cavity  of  the  auricle  itself;^  embolic 

'  Cases  of  extreme  stenosis  are  occasionally  met  with,  more  especially  in  young 
subjects,  in  which  the  hypertrophy  of  the  auricular  wall  continues  good  even  until 
the  end,  and  in  which  the  cavity  of  the  left  auricle  is  very  little  dilated. 

''■  It  occasionally,  though  very  rarely,  happens,  that  the  whole  auricle  becomes 
filled  up  with  a  laminated  clot,  a  narrow  channel  only  remaining  for  the  passage 
of  the  blood  through  it.  Only  one  case  of  this  description  has  come  under  my 
own  observation  ;  in  it  the  aortic  orifice  was  also  diseased  (incompetent),  and 
there  was,  therefore,  in  addition  to  this  mitral  stenosis,  a  further  cause  for  stagna- 
tion and  clotting  in  the  left  auricle. 


Fig.  198.— JlUrai  Stenosis  seen  from  above.    (^Xatural  size.) 

The  cavity  of  the  left  auricle  has  been  cut  open  ;  a  mass  of  calcareous  nodules  (a) 
to  which  some  recent  vegetations  are  attached,  surround  the  constricted  orifice  :  the 
appendix  contains  a  thrombus  (i). 


MnKA«iC<;H>ii.si>n<c'.  Eol 


Pathology  of  Mitral  Stenosis.  481 

symptoms,  are  therefore,  more  apt  to  arise  in  cases  of  mitral 
stenosis  than  in  cases  of  mitral  regurgitation.  The  dilated 
and  permanently  distended  auricle  sometimes  exerts  con- 
tinuous and  injurious  pressure  upon  the  surrounding  parts  ; 
the  left  bronchus  may  for  a  time  be  compressed,  and  collapse 
of  the  left  lung  ma\'  result  from  this  cause. 

In  the  second  place,  mitral  stenosis  is  essentially  a  disease 
of  early  life.  The  compensatory  changes  are,  therefore,  in 
many  cases  much  more  perfect  than  in  the  case  of  mitral 
regurgitation,  which  so  frequently  occurs  in  old  people,  and 
which  is  so  often  due  to  degenerative  changes  in  the  cardiac 
muscle. 

In  the  case  of  mitral  stenosis,  compensation  is  partly 
due  to  hypertrophy  and  dilatation  of  the  left  auricle,  but 
chiefly  to  secondary  hypertrophy  of  the  right  ventricle.  In 
young  healthy  persons  the  right  ventricle  is,  for  a  long  time, 
fully  equal  to  the  strain  which  is  put  upon  it,  and  is  able  to 
propel  the  blood  through  the  lungs,  through  the  left  auricle 
and  through  the  stenosed  mitral  orifice  with  sufficient  force 
to  compensate  the  lesion  ;  compensation  being  of  course 
assisted  by  the  hypertrophy  of  the  left  auricle,  which  also 
occurs.  In  mitral  stenosis  the  systemic  venous  circulation 
may  for  a  considerable  time  be  protected  by  the  hypertrophy 
of  the  right  heart.  The  pulmonary  circulation,  on  the 
contrary,  is  subjected  to  a  severe  strain,  even  in  the  earlier 
stages  of  the  lesion  ;  this  arises  from  the  facts,  (i)  that  the 
obstruction  in  front  is  constantly  present,  i.e.  both  during 
the  diastole  as  well  as  during  the  systole  of  the  left  ventricle, 
and  that  the  suction  action  of  the  left  ventricle,  which  facili- 
tates, as  we  have  already  seen,  the  flow  of  blood  through  the 
lungs,  cannot  be  so  powerfully  exerted  as  in  health  ;  and 
(2)  that  the  hypertrophied  right  ventricle  is  pumping  the  blood 
from  behind  with  increased  force  into  the  pulmonary  circuit. 
In  the  earlier  stages  of  mitral  stenosis,  then,  the  engorgement 
of  the  lungs  is  greater  and  more  continuous  than  in  the  earlier 
stages  of  mitral  regurgitation,  a  fact  which  explains  the  more 
frequent  occurrence  of  haemoptysis  in  stenotic  cases.  So  long 
as  the  hypertrophy  of  the  right  ventricle  is  capable  of  forcing 

H   H 


482  Diseases  of  the  Heart. 

the  blood  through  the  lungs,  and  so  long  as  the  systemic 
venous  system  is  not  much  engorged,  there  is  little  derange- 
ment of  the  general  health,  the  great  functions  of  digestion 
and  assimilation,  excretion  and  inner\-ation,  being  little,  if  at 
all,  interfered  with.  Pulmonary  symptoms  and  complications 
may,  on  the  contrar\-,  be  prominent. 

In  the  ////W/ place,  the  cardiac  contractions,  and  therefore  the 
pulse,  are  not  so  frequent  in  cases  of  mitral  stenosis  as  in  cases 
of  mitral  regurgitation.  In  the  latter  lesion,  a  large  volume  of 
blood  is  being  constantly  sent  backwards  and  forwards  between 
the  cavities  of  the  left  auricle  and  left  ventricle  (the  ventricle 
is,  as  it  were,  playing  at  battledoor  and  shuttlecock  with 
the  auricle,  instead  of  forwarding  all  its  contents  into  the 
aorta),  both  cavities  are  more  quickly  distended,  and,  there- 
fore, contract  more  frequently  than  in  health.  In  the  case  of 
mitral  stenosis,  on  the  contrary,  the  left  auricle  is,  in  con- 
sequence of  permanent  over-distention,  being  more  constantly 
stimulated,  and,  so  long  as  its  muscular  wall  remains  healthy, 
its  contractions  are  more  forcible  and  more  prolonged  than  in 
health  ;  the  left  ventricle,  on  the  contrary,  receives  less  blood 
than  in  the  normal  condition,  it  therefore  requires  less  time 
to  empty  itself  As  a  iiett  result,  the  frequency  of  the  radial 
pulse  is,  in  the  earlier  stages  of  the  case  at  all  events,  not 
increased  as  it  is  in  cases  of  mitral  regurgitation,  indeed  it  is 
sometimes  slower  than  normal  ;  the  tension  of  the  pulse  is, 
too,  in  the  earlier  stages,  much  less  seriously  impaired. 

In  the  fourtJi  place,  the  left  ventricle  does  not  become 
hypertrophied,  as  it  does  in  mitral  regurgitation.  In  fact,  in 
many  cases  of  mitral  stenosis  the  left  ventricle  is  somewhat 
atrophied,  the  diminished  size  of  its  cavity  and  thinning  of 
its  wall  being  due  to  the  facts,  that  it  receives  less  blood  from 
the  auricle,  and  has  less  work  to  do  in  forcing  that  blood  into 
the  aorta,  than  under  normal  circumstances. 

These  remarks,  of  course,  apply  to  cases  of  mitral  stenosis, 
in  which  there  is  little  or  no  mitral  regurgitation.  It  must, 
however,  be  remembered,  that  in  the  majority  of  cases  of  mitral 
stenosis  some  regurgitation  is  present,  and  that  the  amount  of 
this  regurgitation  is  sometimes  considerable.     In  cases  of  this 


Clinical  History  of  Mitral  Stenosis.  483 

description,  the  points  of  distinction  between  mitral  stenosis 
and  mitral  regurgitation,  which  I  have  just  detailed,  may  not 
be  observed.  The  association  of  mitral  regurgitation  with 
stenosis  probably  explains  the  fact,  that  in  some  cases  of 
mitral  stenosis  the  left  ventricle  is  hypertrophied  rather  than 
atrophied.  In  the  later  stages,  hypertrophy  of  the  left  ven- 
tricle may  possibly,  as  Friedreich  has  supposed,  be  due  to  the 
difficulty  which  the  blood  meets  with,  in  passing  from  the 
arterial  into  the  distended  and  engorged  venous  system  ;  or, 
to  venous  engorgement  of  the  wall  of  the  ventricle,  a  con- 
dition which  induces  connective  tissue  overgrowth  and  some 
degree  of  apparent  (false)  hypertrophy.  Again,  in  cases  of 
mitral  stenosis  the  left  ventricle  may  be  hypertrophied  from 
causes  outside  the  heart,  such,  for  example,  as  cirrhosis  of  the 
kidney. 

Clinical  History. — The  onset  of  mitral  stenosis  is,  as  a  rule, 
very  insidious.  In  some  cases  the  condition  is  gradually 
developed  after  an  acute  attack  of  rheumatic  fever  ;  in  others, 
and  these  possibly  constitute  the  majority,  there  are  no  de- 
finite rheumatic  symptoms  or  other  signs  of  acute  illness  to 
mark  the  commencement  of  the  disease. 

Symptoms. — The  compensation  usually  remains  perfect  for 
a  considerable  time,  it  may  be  for  years  ;  and  it  is  only  when 
the  patient  makes  any  extra  exertion,  that  he  feels  short  of 
breath,  suffers  from  palpitation,  and  begins  to  suspect  that  there 
is  something  wrong  with  his  heart.  Pulmonary  complica- 
tions, such  as  bronchial  catarrh  and  haemoptysis  are  of  frequent 
occurrence  even  during  the  stage  of  good  compensation,  and 
result,  as  I  have  already  mentioned,  from  the  engorgement  of 
the  lungs  which  is  usually  present  even  in  the  earlier  stages 
of  the  case.  After  the  failure  of  compensation,  the  systemic 
venous  circulation  becomes  seriously  embarrassed  ;  dropsy 
and  the  other  symptoms,  which  I  have  already  described 
under  the  head  of  mitral  regurgitation  (see  p.  440)  are  then 
developed.  Accidental  symptoms,  due  to  embolic  plugging 
of   some    distant    arterial    trunk,    are    not    uncommon  ;    the 


484  D/scasiS  of  the  Heart. 

embolon  ma)-  be  carried  to  almost  any  part  of  the  body,  but 
the  vessels  which  arc  most  frequently  plugged  are  the  renal, 
splenic,  and  left  iniddle  cerebral  arteries. 

The  exact  nature  of  these  accidental  symptoms  depends, 
of  course,  upon  the  vessel  which  happens  to  be  obstructed, 
and  to  some  extent  upon  the  siz^e  of  the  plug.  Obstniction  of 
the  left  middle  cerebral  artery  causes  right-sided  hemiplegia 
(paralysis  of  the  face,  arm,  and  leg,  on  the  right  side)  and 
aphasia.  Obstruction  of  the  splenic  artery  is  usually  attended 
with  some  pain  in  the  region  of  the  spleen,  which,  on  physical 
examination,  is  found  to  be  enlarged  and  tender  to  the  touch. 
Obstruction  of  the  renal  artery  may  be  attended  with  pain  in 
the  back,  with  albuminuria  or  haematurca.  Obstruction  of  a 
large  branch  supplying  the  intestine  is  generall}'  accompanied 
by  severe  spasmodic  colic,  and  is  sometimes  followed  by 
diarrhoea.  In  each  of  these  cases  there  is  usually,  as  Dr 
Sansom^  and  others  have  pointed  out,  some  elevation  of 
temperature  ;  in  fact,  the  sudden  onset  of  pyrexia  in  a  patient 
who  is  affected  with  mitral  stenosis,  is,  in  the  absence  of  anj- 
obvious  cause,  strongly  suggestive  of  an  embolic  infarction. 

Physical  Signs. — A  presystolic  murmur  having  its  point 
of  differential  maximum  intensit)'  in  the  mitral  area  is,  accord- 
ing to  most  authorities,  pathognomonic  of  mitral  stenosis,"' 
and  is,  therefore,  the  most  important  sign  of  the  disease. 

The  murmur  is  usually  rough  and  rolling,  grinding  or 
churning  in  character.  It  is  almost  exactly  simulated,  as 
Balfour  points  out,  by  the  sounds  which  are  produced  when 
'  the  symbols  Rrrb  or  V^oot  are  vocalised.'  It  occurs  towards 
the  end  of  the  long  pause,  and  ceases  abruptly  with  the  occur- 
rence of  the  first  sound.  It  is  usually  very  localised,  and  is 
best  heard  at  the  left  apex  of  the  heart  or  at  a  point  slightly 

'  Lettsomian  Leclurcs,  p.  93. 

-  Professor  Austin  Flint  differs,  as  I  have  previously  mentioned,  from  this — 
the  usually  accepted  — view  ;  and  thinks  that  a  presystolic  murmur  does  not 
necessarily  indicate  an  organic  lesion  of  the  mitral  valve.  Dr  Sansom  also 
states,  that  in  some  cases  of  aortic  regurgitation  a  presystolic  murmur  is  heard 
at  the  apex  of  the  heart,  but  he  does  not,  so  far  as  I  am  aware,  endorse  the 
opinion  of  Professor  Austin  Flint,  that  it  is  generated  at  the  mitral  orifice. 


Physical  Signs  of  Milral  Stenosis.  485 

within  the  left  apex  ;  it  is  propagated  directly  towards  the 
apex,  and,  therefore,  directly,  as  it  were,  into  the  stethoscope 
and  ear  of  the  observer.     (See  fig.  199.) 


Y\c,.  199. — Outline  I'lgure  ^,hl)\villy  point  of  difterential  maximum  intensity  (*) 
of  the  presystolic  mitral  murmur  (mitral  stenosis) ;  and  the  direction  in  which  it  is 
propagated.  (The  murmur  is  often  best  heard  a  little  above  and  internal  to  the 
apex-beat,  which  in  the  diagram  corresponds  to  the  star.*) 

It  is  important  to  remember  that  this  murmur  is  not 
present  in  all  ca.ses  of  mitral  narrowing.  In  order  that  it  may 
be  produced,  the  conditions  necessary  for  the  formation  of  an 
audible  fluid  vein  must  be  present ;  in  other  words,  the  orifice 
must  be  sufficiently  constricted,  and  the  blood  current  passing 
from  the  left  auricle  to  the  left  \-entricle  must  be  driven 
through  the  constricted  orifice  with  sufficient  force. 

Now,  in  the  earlier  stages  of  mitral  stenosis  {i.e.  in  cases, 
for  example,  in  which  a  slight  degree  of  stenosis  is  found  alter 
death),  a  presystolic  murmur  is  often  absent  owing  to  the  fact 
that  the  orifice  is  not  sufficiently  constricted  to  produce  a  fluid 
vein.  In  cases  of  this  description  the  valve  is  usualh'  incom- 
petent, and,  during  life,  the  case  is  characterised  b\'  the  usual 
symptoms  and  physical  signs  of  mitral  regurgitation. 


486  Diseases  of  the  Heart. 

Again,  in  the  later  stages  of  the  disease,  when  the  left 
auricle  is  much  dilated,  when  its  muscular  wall  is  weak 
and  degenerated,  or  when,  as  in  some  rare  cases,  its  cavit}' 
is  occluded  by  a  thrombus,  the  blood  current  does  not  pass 
through  the  narrowed  orifice  with  sufficient  force  to  produce  a 
fluid  vein  ;  in  these  cases  the  murmur  is  absent. 

It  is,  in  fact,  common  to  meet  with  extreme  constriction  of 
the  mitral  orifice  on  the  post-mortem  table,  which  was  not 
accompanied  b>-  an\-  presystolic  murmur  during  life  (I  mean 
of  course  during  the  later  stages  of  the  case).  Indeed  Dr 
Hilton  Faggc  goes  so  far  as  to  say,  'my  impression  is  that  in 
the  large  majority'  of  the  cases  in  which  mitral  stenosis  is 
found  after  death,  there  is  no  record  of  the  presence  of  a  pre- 
systolic murmur  during  life.'^ 

Again,  in  exceptional  cases,  the  murmur,  instead  of  being 
presystolic,  occurs  during  the  first  part  of  the  diastole  or  long 
pause,  and  is  separated  from  the  first  sound  of  the  heart  by  a 
distinct  inter\-al.     (See  fig.  200.)      In  cases  of  this  description, 


Fig.  200. — Diagrammatic  representatinn  of  post-diastolic  murmur,  which  occurs 
in  some  rare  cases  of  mitral  .stenosis.  It  is  separated  from  the  commencement  of 
the  first  sound  by  an  apprecial)le  interval. 

the  conditions  which  produce  the  passage  of  the  blood  from 
the  cavit}-  of  the  left  auricle  to  the  cavity  of  the  left  ventricle 
at  the  beginning  of  the  ventricular  diastole,  must  be  in  ex- 
cess. Now  these  conditions  are  : — ( i )  the  pressure  of  the  blood 
in  the  cavity  of  the  left  auricle  and  pulmonary  veins  ;  and 
(2)  the  suction  force  which  results  from  the  clastic  recoil  of  the 
left  ventricle  itself  If  either  of  these  forces  were  in  excess, 
the  blood  current  might  pass  through  the  constricted  mitral 
orifice   at  the  commencement  of  the   voitrieular  diastole  with 

'  Russell  Rc'vnohL'  System  of  Mi'Jicir.e,  vol.  iv.  p.  674. 


PJiysical  Signs  of  Alitral  Stenosis.  487 

sufficient  force  to  produce  an  audible  fluid  vein,  which  would 
be  heard  externally  as  a  diastolic  murmur.  The  first  of  these 
conditions,  viz.,  increased  blood  pressure  in  the  left  auricle  and 
pulmonary  veins,  is  probably  the  chief  cause  of  this  form  of 
murmur,  though  the  suction  action  of  the  left  ventricle  cannot 
be  altogether  left  out  of  consideration.^ 

A  presystolic  thrill  can  very  frequently  be  felt  \\hen  the 
hand  is  placed  over  the  position  of  the  apex  beat. 

In  addition  to  the  presystolic  or  diastolic  mitral  murmur 
and  presystolic  mitral  thrill,  which  we  may  term  the  pritnary 
physical  signs  of  mitral  stenosis,  there  are  several  other 
physical  signs  indicative  of  the  altered  condition  of  the  mitral 
segments  and  of  the  secondary  changes  in  the  physical  condi- 
tion and  mode  of  action  of  the  heart.  The  most  important  of 
these  seco7idary  physical  signs,  as  I  am  in  the  habit  of  calling 
them,  are : — 

(i)  Alterations  in  the  character  of  the  first  sound. — The  first 
sound  is  usually  short  and  sharp,  and  rather  resembles  the 
normal  second  than  the  normal  first  sound.  In  some  cases,  it 
has  a  slight  thumping  character,  which  Dr  George  Balfour 
believes  '  is  quite  pathognomonic  (of  mitral  stenosis)  when 
dyly  recognised  by  a  practised  ear,  being  simply  the  last 
portion  of  the  murmur  still  extant,  the  h  of  the  murmur  as 
vocalised  rrrrb,  all  the  R's  being  expunged.'-  In  others,  the 
first  sound  is  replaced  by  a  murmur.  This  is  a  common  con- 
dition, mitral  regurgitation  being  present  as  we  have  previousl)' 
seen,  in  a  considerable  proportion  of  the  cases  of  mitral 
stenosis.  In  those  cases  of  combined  stenosis  and  incom- 
petence in  which  the  stenosis  is  slight,  there  is  only  a  systolic 
murmur  indicative  of  regurgitation.  In  other  cases,  where 
the  stenosis  is  more  considerable,  both  presystolic  and  systolic 
mitral  murmurs  are  present.  In  others  again,  a  presystolic 
murmur  is  present,  but  no  systolic  murmur. 

'  When  this  chapter  was  written  I  had  not  read  Dr  Galaliin's  instructive  paper 
on  the  Cardiograph  in  Guy's  Hospital  Reports,  1875,  p.  261.  In  that  paper  he 
very  clearly  points  out  the  causation  of  murmurs  of  this  description,  and  also  states 
that  r3r  Fagge  explained  their  occurrence  by  the  auricular  contraction  occurring 
immediately  after,  instead  of  immediately  before,  the  ventricular  systole. 

•   Diseases  of  Heart,  \s.  139.  ^ 


488  Diseases  0/  the  Heart. 

(2)  RaiuplicatioH  of  the  second  sound.— TMx-^  condition, 
which  is  diagrammatically  shown  in  fig.  201,  is  probably 
present  in  at  least  one-third  of  all  the  cases  of  mitral  stenosis, 
and  is  of  considerable  diagnostic  value.  The  different  views 
which  have  been  advanced  to  explain  its  production,  need 
not  be  again  detailed.     (See  p.  162.) 


Fig.    20\.— Diagrammatic  representation  of  the  munntir  and  reduplicated 
second  sound  in  mitral  stenosis. 

(3)  Accentuation  of  the  pulmonary  second  sound. — This  is 
a  most  important  physical  sign  in  cases  of  mitral  stenosis,  for 
it  is  to  some  extent  a  measure  or  gauge  of  the  extent  of  the 
mitral  lesion.  But  this  point  will  be  more  appropriately  con- 
sidered under  the  prognosis. 

(4)  Physical  signs  xvhich  are  due  to  alterations  in  the  size 
and  shape  of  the  heart. — The  left  apex  is  usually  ill  defined  a^d 
indistinct,  but  is  not  displaced  downwards  and  outwards  as  it 
is  in  mitral  regurgitation  ;  an  exception,  of  course,  occurs  in 
those  cases  of  mitral  stenosis  in  which  the  left  ventricle  is 
hypertrophied  either  as  the  result  of  intrinsic  or  extrinsic 
causes  ;  cases  of  this  description  are  however  rare.  Dulness, 
or  rather  an  impaired  percussion  note  is  sometimes  present 
over  the  area  of  the  dilated  left  auricle,  viz.,  in  the  second  and 
third  left  interspaces  ;  it  is,  I  think  generally  derived  from 
the  dilated  conus  arteriosus  of  the  right  ventricle  and  from 
the  dilated  pulmonary  artery,  rather  than  from  the  dilated  left 
auricle,  which  is  more  deeply  situated  in  the  chest. 

Pulsation  can  also  in  some  cases  be  felt  in  the  second  and 
third  left  interspaces.  Some  authorities  believe  that  this  pulsa- 
tion is  derived  from  the  dilated  left  auricle,  or  from  its  dilated 
appendix  ;  a  more  probable  view  is  that,  I  think,  which 
supposes  that  it  is  produced  by  the  dilated  pulmonary  artery 


Physical  Signs  oj  Miti'al  Stenosis.  489 

or  dilated  and  displaced  conus  arteriosus  of  the  right 
ventricle. 

Hypertrophy  and  dilatation  of  the  right  ventricle,  tricuspid 
incompetence,  and  dilatation  of  the  right  auricle,  are  of 
frequent  occurrence  in  the  later  stages  of  mitral  stenosis  ; 
and  give  rise  to  increased  dulness,  and  other  physical  signs, 
which  I  shall  afterwards  describe  more  in  detail. 

(5)  The  cJiaracters  of  the  cardiograpJiic  traeing. — In  many 
cases  of  mitral  stenosis  the  cardiograph  affords  very  important 
information.     The  chief  alterations  are  as  follows  : — 

{a)  The  duration  of  the  diastolic  portion  of  the  tracing  is 
prolonged  in  consequence  of  the  fact  that  the  over-distended 
left  auricle  requires  a  longer  time  than  usual  to  discharge  its 
contents  into  the  cavity  of  the  left  ventricle.  (See  figs.  202, 
203,  204,  205.) 

{b)  When  the  stenosis  is  not  very  great,  there  is  usually  a 
very  marked  rise  immediately  after  the  wave  k,  which  indicates 
the  diastolic  relaxation  of  the  ventricle,  in  consequence  either 
of  the  fact  that  the  tension  of  the  blood  in  the  left  auricle 
and  pulmonary  veins  is  greater  than  normal,  and  the  blood 
flow  from  this  auricle  to  the  ventricle,  at  the  commencement 
of  the  ventricular  diastole,  is  more  forcible  than  in  health  ; 
or,  as  some  have  supposed,  that  the  auricular  contraction 
commences  earlier  than  usual.     (See  figs.  202,  203,  204.J 


Fig.   202.  —  Cardiograpliic  tracing  in  a  case  of  mitral  stenosis. — {After  Galahin.) 

'  Henry  A.,  ret  8.  Systolic  and  long,  harsh  presy'stolic  murmurs  at  the  ape.\, 
both  accompanied  by  thrill.  The  presystolic  murmur  commenced  immediately 
from  the  second  sound,  and  was  separated  by  a  short  pause  from  the  systole.  The 
bracket  in  the  figure  represents  the  duration  of  the  murmur,  which  is  separated 
by  a  distinct  interval  from  the  ventricular  systole.  The  letter  a,  indicates  the 
greatest  auricular  contraction.'' — (Gny^s  Hospital  A\forts,  1S75,  p.  3H-) 

'  For  the  e.xact  significance  of  the  other  letters  and  parts  of  the  tracing,  the 
reader  is  referred  to  the  appendix. 


490 


Disease's  of  the  Heart. 


Fin.   loi.  —  Cardiographic  /racing  in  a  case  of  mitral  stenosis.— {After  Galabin.) 

'George  M.,  ret.  19.     Long,  loud,  and  harsh  presystolic  inurmiir,  commencing 

immediately  from  the  second  sound  and  running  up  lo  the  first  sound.      Pulse  60. 

The  letter  a,  indicates  the  probable  commencement  of  the  auricular  contraction.' — 

{Guys  Hospital  Reports,  1S75,  p.  314.) 


Fig.   204. — Cardiographic  tracing  in  a  case  of  mitral  stenosis. — [After  Galabin.) 

'Matilda  A.,  jet.  37.  Long,  rough,  presystolic  murmur,  commencing  imme- 
diately from  the  second  sound,  and  leading  up  to  the  first  sound.  Pulse  57.' — 
{Guy's  Hospital  Reports,  1875,  p.  314. ) 

{/)  In  those  cases  in  which  the  stenosis  is  not  great,  and  in 
which  the  muscular  wall  of  the  left  auricle  is  hypertrophied, 
the  wave  a,  which  indicates  the  auricular  contraction,  is  in- 
creased in  height  and  its  base  widened,  in  consequence  of  the 
fact  that  the  contraction  of  the  hypertrophied  auricle  is  more 
forcible  and  lasts  longer  than  under  normal  circumstances. 
(See  fig.  202.)  In  some  cases  the  auricular  wave,  instead  of 
immediately  preceding  the  rise,  which  marks  the  commence- 
ment of  the  \'entricular  systole,  occurs  in  the  earlier  part  of 
the  diastolic  portion  'of  the  tracing,  owing  to  the  fact  that  the 
rhythm  of  the  auricular  contractions  is  altered.  (See  fig.  203.) 
When  the  stenosis  is  great,  the  enlargement  of  the  auricular 
wave  is  not  observed,  for  the  auricular  contraction  (even  when 
the  auricular  wall  is  h\'pertrophicd,  and  it  is  often  dilated  and 
weak  rather  than  hypertrophied  in  cases  of  this  description)  is 
unable  to  propel  a  sufficiently  large  quantity  of  blood  through 


Physical  Signs  of  Mitral  Stenosis.  491 

the  narrow  orifice  to  produce  a  distinct  wave  in  the  cardio- 
graphic  tracing.  When  the  auricular  wall  is  dilated  rather 
than  hypertrophied,  the  size  of  the  auricular  wave  is  dimi- 
nished rather  than  increased,  whatever  be  the  condition  of 
the  mitral  orifice.  The  auricular  wave,  then,  will  only  be 
exaggerated  in  those  cases  of  mitral  stenosis  in  which  the 
auricular  wall  is  capable  of  contracting  powerfully,  and  in 
which  the  stenosis  is  not  too  great  to  prevent  this  effect  of 
the  auricular  contraction  being  manifested  in  the  cardio- 
graphic  tracing. 

{d)  The  diastolic  portion  of  the  tracing  is  in  some  cases 
interrupted  by  a  series  of  elevations  and  depressions,  indica- 
tive of  the  vibrations  which  are  heard  as  a  murmur  or  felt  as 
a  thrill  in  the  mitral  area.  (See  figs.  202,  203,  and  204.) 
These  vibrations  are  usually  presystolic,  but  in  some  cases 
they  are  separated  by  a  distinct  interval  from  the  up-stroke, 
which  represents  the  commencement  of  the  ventricular  systole. 
(See  fig.  202.) 

{e)  The  systolic  portion  of  the  tracing  does  not,  as  a  rule, 
present  any  special  features.  When  the  stenosis  is  consider- 
able, or  the  left  ventricle  dilated,  the  initial  rise  which  marks 
the  commencement  of  the  ventricular  systole  is  followed  by  a 
more  rapid  fall  than  in  health.  (See  figs.  202,  203,  and  204.) 
In  other  cases,  more  especially  when  the  left  ventricle  is 
powerful  or  hypertrophied,  the  systolic  portion  of  the  tracing 
is  sustained  and  broad.     (See  fig.  204.) 

{f)  The  irregularity  in  the  sequence  of  the  ventricular 
contractions,  which  is  best  demonstrated  by  means  of  the 
sph}'gmograph,  is  also  seen  in  cardiographic  tracings.  (See 
fig.    204.)     The    cardiograph    also    seems    to    show    that    in 


Fig.   205. —  Cardio};rap]iic  trafiiit;-  in  a  case  of  mitral  stenosis. — [After  Sansoiii.) 

The  tracing  was  taken  by  Pond's  cardiograph.  A  loud,  rolling,  or  bubbling 
presystolic  murmur  at  the  apex  :  the  irregularity  of  successive  ventricular  contrac- 
tions is  well  seen.  ~  Diagnosis  of /diseases  of  the  Heart,  p.  271. 


492  Dist'dses  of  the  Heart. 

some  cases  the  normal  sequence  of  the  cardiac  contractions 
is  so  altered  that  some  of  the  auricular  contractions  are 
not  followed  b\'  xentricular  contractions,  as  is  normally  the 
case. 

(6)  Altcratious  in  t/ie  character  of  tlie  pulse. — The  character 
of  the  pulse  in  mitral  stenosis  depends  upon  the  degree  of  con- 
striction and  the  condition  of  the  muscular  tissue  of  the  heart, 
more  especially  of  the  left  auricle. 

When  the  stenosis  is  great,  the  pulse  is  smaller  than 
normal  in  consequence  of  the  fact  that  the  left  ventricle 
has  less  blood  to  expel  into  the  arterial  system  than  under 
ordinary  circumstances.  So  long  as  the  left  auricle  is  able 
to  empty  itself,  i.e.  so  long  as  hypertrophy  predominates 
o\er  dilatation,  the  pulse  may  be  of  good  volume,  good 
tension,  and  perfectly  regular,  but  it  usually  happens  that 
in  consequence  of  over  distention  the  muscular  tissue  of  the 
left  auricle  is  every  now  and  again  stimulated  to  premature 
contraction,  which  passing  to  the  muscular  tissue  of  the 
ventricle,  is  m'anifested  at  the  wrist  in  the  form  of  an  im- 
perfect pulsation — a  small  pulse  wave,  as  it  were,  interposed 
between  two  normal  beats.  (See  fig.  206.)  The  small  imper- 
fect   pulse   wave   seems    to   occur    during    the    down-stroke 


Flc.  206. — Pulse  tracing  in  .Mitral  Stenosis. 

The  compensation  is  still  fairly  good,  a  second  small  pulse  wave  is  seen  in  the 
down  stroke  of  the  third  beat. 

of  the  previous  beat.  In  the  later  periods  of  the  case,  and 
especially  when  the  cavity  of  the  left  auricle  is  constantly 
over-distended  and  its  muscular  fibre  in  a  condition  of  irri- 
table weakness,  the  pulse  becomes  quick  and  extremely 
irregular,  the  irritable  muscle  discharging,  as  it  were,  at  rapid 


Diagnosis  of  Mitral  Stenosis.  493 

and  irregular  intervals  under  the  continuous  stimulus  to  which 
it  is  subjected  in  consequence  of  the  increased  blood  pres- 
sure within  the  auricular  cavity. 

Diagnosis. — When  a  case  of  suspected  mitral  stenosis  comes 
before  us  we  must  endeavour  to  determine : — 

(i)  Is  mitral  stenosis  actually  present  ? 

(2)  If  mitral  stenosis  is  present,  what  is  the  exact  extent 
and  severity  of  the  lesion  ? 

Step.  No.  I. — Is  mitral  stenosis  actuaily  present  ? 

It  is  often  impossible,  as  I  have  previously  pointed  out,  to 
distinguish  slight  degrees  of  constriction  of  the  mitral  orifice 
during  life.  In  cases  of  this  description,  there  is  no  distinctive 
evidence  of  stenosis  ;  the  mitral  valve  is  generally  incompe- 
tent as  well  as  slightly  constricted,  and  the  case  presents  the 
usual  features  of  mitral  regurgitation.  In  some  cases  of  this 
description  the  cardiograph  will  probably  afford,  as  Dr 
Sansom  has  suggested,  important  information  ;  when  stenosis 
is  combined  with  incompetence  the  diastolic  portion  of  the 
cardiographic  tracing  is  more  prolonged  than  in  those  cases 
in  which  regurgitation  is  the  only  lesion. 

Passing  to  those  cases  in  which  the  constriction  is  more 
considerable,  we  find,  that  in  some  the  diagnosis  is  extremely 
ea.sy,  in  others  difficult. 

In  those  cases  in  which  a  presystolic  murmur,  having  its 
point  of  differential  maximum  intensity  in  the  mitral  area, 
and  presenting  the  rough  rolling  character  previously  described, 
is  present,  the  diagnosis  is  self-evident.  Such  a  murmur,  so 
far  as  my  observation  goes,  is  pathognomonic  of  mitral 
stenosis.^ 

The  murmur  is  not,  however,  aK\a}'s  typical  ;  in  some 
cases,  for  example,  it  is  not  presystolic,  but  occurs  at  the 
commencement  of  the  diastole,  and  is  separted  from  the 
ventricular  systole  by  a  distinct  interval  ;  in  other  cases  it  is 
absent  altogether.  In  some  cases,  too,  it  is  simulated  by  the 
murmur  of  aortic  regurgitation.  This  is  most  likely  to  be  the 
case,  as  Dr  Sansom  points  out,  when    the  murmur  of  aortic 

'  II  must  not,  however,  be  forgotten  that  Or  Austin  Flint  holds  p.  different  view. 


494  Diseases  of  tJic  Heart. 

regurgitation  is  conducted  towards  the  apex,  and  especially, 
as  is  sometimes  the  case,  when  it  is  heard  only  in  the  mitral 
area.  '  Cases  have  been  recorded,'  says  Dr  Sansom,  '  in  which 
a  presystolic  murmur  has  been  noted  during  life,  and  the 
autopsy  has  demonstrated  not  mitral  stenosis  but  aortic 
regurgitation.'^ 

We  must  not,  therefore,  rely  upon  the  mere  rhythm  of  the 
murmur  alone,  but  must  base  our  diagnosis,  as  we  should 
always  base  it,  on  all  the  facts  of  the  case.  We  must  observe 
the  sound  characters  of  the  murmur,  the  shape  and  outline  of 
the  heart  as  a  whole  and  of  its  component  parts,  the  condition 
of  the  pulmonary  second  sound,  and  the  exact  characters 
of  the  pulse.  If  these  points  are  accurately  noted,  there 
should  be  no  difficulty  in  distinguishing  aortic  incompetence 
from  mitral  stenosis,  even  in  those  cases  in  which  the  murmur 
is  only  heard  at  the  apex,  and  is  more  or  less  presystolic  ;  for 
the  secondar>'  alterations  in  the  heart  and  circulation,  which 
result  from  aortic  incompetence,  are  totally  different  from  those 
caused  by  mitral  constriction.     (See  pp.  480  and  505.) 

Those  cases  in  which  the  murmur  is  wanting  altogether, 
present  greater  difficulties.  A  patient,  for  example,  comes 
under  obser\-ation  suffering  from  dropsy  of  the  feet  and  lower 
extremities,  shortness  of  breath  and  cough  ;  he  is  markedly 
cyanotic,  the  right  heart  enlarged,  the  tricuspid  valve  perhaps 
incompetent,  the  second  sound  reduplicated,  the  pulmonary 
second  sound  markedly  accentuated,  the  pulse  quick,  small, 
weak,  and  irregular.  There  is  no  murmur  in  the  mitral  area, 
the  left  apex  is  ill  defined,  but  is  not  displaced  outwards 
and  to  the  left.  The  lungs  are  markedly  emphysematous, 
the  normal  respiratory  sounds  are  replaced  by  bronchitic 
rales. 

Bronchitis  and  emphysema,  with  extensive  secondary 
changes  in  the  right  heart,  are  evidently  present,  but  it 
may  be  extremely  difficult  or  even  impossible  to  decide 
whether  these  conditions  are  primary  or  secondary  to  a  con- 
striction of  the  mitral  orifice.  It  is  only  by  careful  atten- 
tion to  the  history  of  the  case  that  the  point  can  be  decided 

'  Le/isoiitian  Lectures,  p.  70. 


Diagnosis  of  Miti'al  Stenosis.  495 

with  any  approach  to  certainty.  A  history  of  rheumatism, 
especially  of  articular  rheumatism  ;  of  shortness  of  breath 
on  exertion,  the  dyspnoea  having  gradually  and  steadily  in- 
creased, and  being  present  on  exertion,  whether  the  patient 
was  suffering  from  '  cold '  (bronchitis)  or  not,  is  suggestive  of 
mitral  constriction  ;  vice  versa  when  there  is  no  rheumatic 
history,  when  the  patient  has  suffered  from  repeated  attacks 
of  bronchitis,  when  the  shortness  of  breath  has  not  steadily 
and  gradually  increased,  and  especially  if  there  have  been 
intervals  (between  the  attacks  of  bronchitis)  in  which  his 
'wind'  was  pretty  good,  the  probability  of  primary  lung 
disease  and  the  absence  of  mitral  stenosis  are  indicated.^ 

In  some  cases  of  cirrhosis  of  the  lung  with  secondary 
hypertrophy  and  dilatation  of  the  right  heart,  the  same  diffi- 
culty in  diagnosis  occurs. 

In  those  cases  of  advanced  mitral  disease  in  which  there 
is  no  murmur,  and  in  which  pulmonary  complications  (bron- 
chitis, emphysema,  cirrhosis,  etc.)  are  present  in  small  degree 
or  altogether  wanting,  the  diagnosis  can  be  made  with  much 
greater  facility.  In  cases  of  this  description  the  accentuated 
pulmonary  second  sound  and  the  hypertrophied,  or  hyper- 
trophied  and  dilated  right  heart  show,  that  there  is  some 
obstruction  to  the  passage  of  the  blood  through  the  lungs  ; 
and  if  there  is  no  evidence  of  primary  lung  disease  (emphy- 
sema, cirrhosis,  etc.)  sufficient  to  produce  the  obstruction,  we 
may  with  some  confidence  conclude  that  the  cause  of  the 
obstruction  is  placed  at  the  mitral  orifice. 

Careful  cardiographic  observations  would  probably  help  us 
in  distinguishing  these  cases.  The  character  of  the  pulse  too, 
is,  I  think,  of  some  importance.  In  advanced  mitral  con- 
striction the  pulse  is  more  likely  to  be  irregular  than  it  is  in 
bronchitis  and  emphysema  and  in  the  other  primary  lung 
affections  in  which  the  difficulty  in  diagnosis,  which  we  are 
now  considering,  is  likely  to  occur. 

Cases,  in  which  haemoptysis  occurs  as  an  early  symptom, 

'  Cases  of  this  description,  in  which  the  attacks  of  bronchitis  date  back  from 
childhood,  are  often  attended  with  extreme  cyanosis,  and  are  likely  to  be  mistaken 
for  cases  of  congenital  malformation  of  the  heart. 


496  D!sc(7scs  of  tJic  Heart. 

may  be  mistaken  for  commencing  phthisis.  I  remember 
making  a  mistake  of  this  kind  soon  after  commencing  practice, 
which  I  have  never  forgotten.  A  young  man  consulted  me 
for  hremoptysis  ;  he  was  thin  and  spare  ;  some  bronchial  rales 
and  a  well-marked  presystolic  mitral  murmur,  were  present. 
The  breathing  at  the  right  apex  was  a  little  harsher  than  at 
the  left  (a  condition  which  is,  of  course,  quite  compatible  with 
perfect  health).  I  erroneously  attributed  the  hsemoptysis  to 
primary  lung  disease,  an  opinion  which  was  shortly  afterwards 
very  properly  set  aside  by  the  late  Dr  Murchison.  The  patient 
is,  I  believe,  still  aliv^e,  and  has  never  had  any  symptoms 
or  signs  of  phthisis.  Cases  in  which  the  same  mistake  is 
committed  are  by  no  means  uncommon,  and  more  than  one 
has  since  come  under  my  own  personal  observation. 

Step  No.  2.  If  the  case  is  one  of  mitral  stenosis,  zu/iat  is  the 
extent  and  gravity'  of  the  lesion  ? 

This  step  in  the  diagnosis  will  be  more  appropriately  con- 
sidered under  the  prognosis,  to  which  I  now  pass. 

Prognosis. — Having  decided  that  the  case  is  one  of  mitral 
stenosis,  we  must  endeavour  to  determine  what  is  the  gravity 
of  the  lesion.  Here,  as  in  the  case  of  mitral  regurgitation,  the 
extent  and  gravity  of  the  lesion  are  not  altogether  synony- 
mous terms.  The  gravity  of  the  lesion  is,  in  short,  determined 
by  observing  : — 

I.  The  degree  or  amount  of  the  stenosis.  We  form  an 
opinion  on  this  point  by  showing  —  [a)  the  extent  of  the 
secondary  changes  produced  in  the  heart  itself ;  and  {b)  the 
amount  of  mechanical  derangement  produced  in  the  arterial 
and  venous  systems  respectively.  The  extent  of  the  hyper- 
trophy and  dilatation  of  the  right  heart  is  the  most  important 
guide  to  the  extent  of  the  mitral  lesion.  The  degree  of 
accentuation  of  the  pulmonary  second  sound  is  also  of  great 
value,  more  especially  in  the  earlier  stages  of  the  case.  In 
attempting  to  gauge  the  extent  of  the  constriction  by  the 
loudness  of  the  pulmonary  second  sound,  it  is  important 
to  take  into  account  the  condition  of  the  lungs  on  the  one 
hand,  and  of  the  right  ventricle  on  the  other.     Accentuation 


Prognosis  of  Mitral  Stenosis.  497 

of  the  pulmonary  second  sound  is  onl}-,  of  course,  an  indica- 
tion of  increased  blood-presssure  in  the  puhnonary  artery  ; 
and  since  increased  pulmonary  tension  may  be  due  to  pulmon- 
ary causes  (such  as  bronchitis  and  emph}'sema),  the  exact 
condition  of  the  lungs  must  be  accurately  determined  before 
we  can  attempt  to  measure  the  degree  of  the  mitral  stenosis 
by  the  extent  of  the  accentuation  of  the  pulmonary  second 
sound  which  is  present.  Again,  it  is  essential  to  remember, 
that  the  degree  of  the  pulmonary  tension,  and  therefore  the 
loudness  of  the  pulmonary  second  sound,  depend  upon  the 
condition  of  the  right  ventricle.  W'ith  the  same  amount 
of  obstruction  in  front,  the  pulmonary  second  sound  will  be 
much  louder  when  the  ventricle  is  hypertrophied  and  acting 
powerfully  than  when  it  is  dilated  and  acting  feebl}-.  The 
mere  loudness  of  the  pulmonary  second  sound  is  not,  there- 
fore, any  accurate  guide  to  the  extent  of  the  mitral  con- 
striction, unless  we  at  the  same  time  take  into  account  the 
condition  of  the  lungs  and  of  the  right  heart. 

2.  The  capabilities  of  compensation  and  the  powers  of 
resistance  possessed  b}-  the  particular  patient  under  observa- 
tion. 

3.  Whether  the  lesion  of  the  mitral  valve  is  progressive  or 
stationary'. 

4.  The  presence  or  absence  of  complications. 

The  same  remarks  which  have  previously  been  made  with 
regard  to  headings  2,  3,  and  4,  in  speaking  of  the  prognosis  of 
mitral  regurgitation  apply  here.     (See  page  459,  et  seq.) 

Treatuicnt. — In  treating  cases  of  mitral  stenosis,  the  in- 
dications are  the  same,  and  the  methods  of  treatment  are 
similar  to  those  which  have  been  described  as  suitable  in 
cases  of  mitral  regurgitation.  (See  page  467.)  I  need  not 
again  enter  into  details,  but  must  once  more  emphasise  the 
statement,  that  in  the  earlier  stages,  and  so  long  as  compensa- 
tion is  perfect,  little  or  no  drug  treatment  is  required. 


II 


498  Diseases  of  tJte  Heart. 

AORTIC  IXCOMPETEN'CE. 
Definition.— Aortic  incompetence  includes  all  those  condi- 
tions which  interfere  with  the  perfect  closure  of  the  aortic  valve, 
and  allow  a  regurgitant  current  to  pass  from  the  aorta  into  the 
cavity  of  the  left  ventricle  during  the  ventricular  diastole. 

Aitiology  and  Pathology.— Pvoxtxc  regurgitation  is  a  common 
condition,  though  not  nearly  so  common  as  mitral  regurgita- 
tion. It  is  comparatively  seldom  met  with  in  young  persons, 
but  is  of  most  frequent  occurrence  during  active  manhood  and 
the  later  periods  of  life.  It  is  much  more  common  in  men 
than  in  women,  a  circumstance  which  is  explained  by  the  fact 
that  the  root  of  the  aorta  and  aortic  valve  segments  are  more 
subjected  to  strain,  and  are  more  liable  to  be  affected  with 
atheroma  and  chronic  inflammation  in  the  male  than  in  the 
female. 

In  order  to  comprehend  intelligently  the  diseases  of  the 
aortic  valve,  it  is  essential  to  remember  that  it  (the  valve) 
forms  a  barrier  between  the  arterial  system,  on  the  one  hand, 
and  the  heart,  on  the  other  ;  and  that  the  morbid  processes 
which  produced  lesions  of  the  aortic  segments  arise  in  some 
cases  in  the  base  of  the  aorta,  in  others,  in  the  endocardial 
lining  membrane  of  the  heart.  Further,  it  is  all  important 
to  bear  in  mind,  that  the  force  with  which  the  aortic  valves 
are  closed,  depends  upon  the  condition  of  the  aortic,  i.e.  of  the 
systemic  arterial  blood-pressure.  But  in  order  that  these 
points  may  be  thoroughly  understood,  I  must  now  describe  in 
detail  the  anatomical  construction  of  the  aortic  segments,  and 
the  exact  manner  in  which  their  closure  is  effected. 

The  aortic  orifice  is  circular  in  form,  and  the  aortic  valve 
consists  of  three  semi-lunar  flaps  ;  each  flap  is  attached  by 
its  convex  border  to  the  side  of  the  artery  at  the  place  where 
it  joins  the  ventricle,  whilst  its  other  border,  which  is  nearly 
straight,  is  free,  and  projects  into  the  interior  of  the  vessel. 
The  segments  of  the  valve  are  composed  of  fibrous  tissue, 
covered  by  a  prolongation  of  the  endocardium  on  the  one 
side,  and  of  the  inner  coat  of  the  aorta,  on  the  other.     The 


y^tiology  and  Pat Jiology  of  Aortic  Incompetence.   499 

thickness  of  the  segments  varies  in  different  parts.  A  tend- 
inous band  strengthens  the  free  edge  of  the  flap,  and  at  the 
middle  of  the  free  edge  there  is  a  sHght  fibro-cartilaginous 
thickening,  the  iiodiiliis  or  corpus  Arantii.  Other  tendinous 
fibres,  arising  from  the  attached  border,  run  in  the  valve  to- 
wards the  nodule,  occupying  its  whole  extent,  except  two 
narrow  lunulated  portions,  one  on  each  side  adjoining  the  free 
margin  of  the  valve.  These  parts,  which  are  named  lunulce, 
are  therefore  thinner  than  the  rest.  There  is  also  a  strength- 
ening fibrous  cord  surrounding  the  attached  border  of  each 
valve.  The  wall  of  the  aorta  is  bulged  out  opposite  each 
semi-lunar  flap  ;  these  bulgings  are  known  as  the  sinuses  op 
Valsalva.     (See    fig.    207.)     One    of  the    sinuses    is  situated 


Fk;.  207. — Po!-tio7i  0/ the  aorta  and  wall  of  the  left  ventricle  ivith  one  entire 
segment  and  two  half  segments  of  the  aortic  valve. — {After  Quain.) 

a,  b,  c,  sinuses  of  Valsalva  opposite  the  segments ;  in  a,  and  b,  the  apertures 
of  the  coronary  arteries  are  seen  ;  d,  d ,  the  inner  surface  of  the  wall  of  the  ven- 
tricle;  I,  2,  curved  attached  border  of  the  segments;  3,  the  middle  of  the  free 
border  (corpus  Arantii). 

anteriorly,  the  other  two  posteriorly.  The  right  coronary 
artery  arises  from  the  anterior  sinus,  and  the  left  coronary 
artery  from  the  left  posterior  sinus.  The  right  posterior  sinus 
is  sometimes  called  the  intercoronary  sintis} 

The  action  of  the  valve  is  as  follows  : — when  the  left  ven- 
tricle contracts  the  valve  segments  are  burst  open,  but  do  not 


'   Quain^s  Anatomy,  vol.  ii.  p.  490. 


500  Diseases  of  the  Heart. 

come  into  immediate  contact  with  the  aortic  wall,  as  was  at 
one  time  supposed  ;  they  seem  to  be  retained  (probably  as  the 
result  of  reflux  currents  passing  round  the  root  of  the  aorta 
and  into  the  sinuses  of  Valsalva)  in  an  intermediate  position  ; 
the  orifice  of  the  valve,  when  it  is  opened,  is  more  or  less 
triangular  in  shape.  As  soon  as  the  contraction  of  the  left 
ventricle  ceases,  the  pressure  behind  the  valve  becomes 
negative  ;^  reflux  currents  at  the  root  of  the  aorta  are 
produced,  which  float  the  segments  of  the  valve  into  close 
apposition.  The  elastic  recoil  of  the  aorta  then  occurs,  the 
root  of  the  aorta  including,  of  course,  the  sinuses  of  Valsalva, 
is  bulged  out,  the  valve  flaps  are  tensely  stretched,  and  are 
brought  into  firm  and  accurate  contact.  It  must  also  be 
remembered  that  the  strain  of  this  forcible  closure  is  borne  by 
the  corpora  Arantii  and  tough  fibrous  portions  of  the  valve 
flaps,  and  that  the  delicate  luiiulce  are  not  subjected  to  any 
strain,  but  are  simply  pressed  against  each  other,  so  as  most 
effectually  and  completely  to  close  the  orifice. 

Now  aortic  incompetence  may  be  due  either  to  : — 

1.  Alterations  of  the  valve  segments,  which  prevent  their 
perfect  adaptation  and  closure; 

2.  Dilatation  of  the  base  of  the  aorta,  the  valve  segments 
being  health}'.  This,  which  is  a  rare  condition,  is  termed 
relative  incompetence.  Let  us  now  shortly  consider  each  of 
the  pathological  causes  of  these  two  forms  in  detail. 

Alterations  in  the  valve  segments,  which  prevent  their  perfect 
adaptation  and  closure,  may  be  due  to : — 

I.  Congenital  malformation,  or  disease  in  intra-uterinc  life. 
— This  is  an  extremely  rare  cause  of  aortic  incompetence, 
though  congenital  malformation  of  the  valve  segments  is  not 
uncommon.     In  some  cases  of  congenital  malformation  there 

'  Foster  states  that  '  when  in  a  closed  channel  a  rapid  current  suddenly  ceases, 
a  negative  pressure  makes  its  appearance  in  rear  of  the  fluid,  and  sets  up  a  reflux 
current.  So  when  the  last  portions  of  blood  leave  the  ventricle  a  negative  pres- 
sure makes  its  appearance  behind  them  in  the  ventricle,  and  leads  to  a  reflux  cur- 
rent from  the  aorta  towards  the  ventricle.' — [Text-Book  of  Physiology,  p.  143.) 
The  elastic  recoil  of  the  ventricle  produces  also,  as  we  have  previously  seen, 
considerable  negative  pressure  in  the  ventricular  cavity,  which  must  contribute 
very  materially  to  the  production  of  these  reflux  currents. 


Etiology  and  Pathology  of  Aortic  Incompetence.    501 

are  only  two  segments,  in  others  more  than  three,  but  in  the 
majority  of  cases  of  this  description  the  valve  is  competent, 
and  it  is  only  by  accident  the  condition  is  discovered  after 
death.  It  must,  however,  be  remembered  that  malformed 
valves  seem  more  liable  to  be  attacked  by  endocarditis  in  later 
life  than  naturally  formed  ones.  In  other  cases  the  number 
of  segments  is  normal,  but  adjacent  flaps  are  adherent  at  their 
edges.  In  some  cases  of  this  description,  in  which  the  valve 
has  become  incompetent  in  later  life,  it  has  been  supposed 
that  the  adhesions  were  due  to  intra-uterine  disease. 

2.  Traninatic  rupture  of  the  valve  flaps. — Rupture  of  the 
aortic  segments,  as  the  result  of  traumatic  injury  or  sudden 
effort,  is  extremely  rare  in  perfectly  healthy  individuals.  It  is 
probable  that  in  many  cases  in  which  a  valve  flap  has  given 
way  under  sudden  effort  or  strain,  it  was  weakened  by  previ- 
ous disease,  which  had  not  advanced  sufficiently  far  to  give 
rise  to  symptoms.  Rupture,  the  result  of  ulcerative  inflam- 
mation, is  of  course  more  common.  (See  figs.  168  and  169.) 
In  both  forms  of  rupture  the  regurgitation  is  usually  very 
free  ;  cases  of  this  description  generally  run  a  rapid  course, 
and,  so  far  as  we  know,  are  invariably  fatal.  In  the  follow- 
ing case,  in  which  the  rupture  was  possibly  partly  due  to 
strain,  but  chiefly  to  ulceration,  the  patient  survived  for  a 
considerable  time  : — 

Case. — J.  R.,  iet.  36  (height  5  ft.  y^  in.,  weight  when  in  heaUh, 
12  St.  12  lbs.),  an  extremely  powerful  man,  was  admitted  to  the  Newcastle- 
on-Tyne  Infirmary  under  my  care  on  November  12th  1874.- 

The  /listory  which  he  gave  of  the  commencement  of  the  case,  was 
interesting,  and  was  as  follows  : — He  stated  that  with  the  exception  of  a 
cough,  from  which  he  had  suffered  for  some  two  years  before  his  present 
ilhiess  commenced,  he  had  enjoyed  excellent  health,  never  having  been 
in  bed  from  illness  for  a  single  day.  One  morning  at  the  end  of  June 
1874,  he  noticed  a  peculiar  noise  on  getting  out  of  bed  in  the  morning  ; 
he  thought  it  proceeded  from  under  the  bed,  but  failing  to  find  any  cause 
for  it  there,  and  after  searching  the  other  parts  of  his  house  and  finding 
that  it  always  accompanied  him,  he  concluded  that  it  originated  inside 
his  own  body.  On  consulting  a  doctor  he  was  told  it  proceeded  from 
his  heart.  Before  the  noise  commenced,  he  had  been  engaged  on  'a  very 
heavy  job  lifting  stones,'  but  was  not  aware  that  he  had  strained  himself 
For  some  weeks  after  the  noise  was  first  noticed,  he  was  able  to  continue 


502  Diseases  of  tJic  Heart. 

his  ordinar)-  employment-  that  of  a  labourer.  He  then  caught  cold  and 
became  short  of  breath  The  shortness  of  breath  and  cough  gradually 
increased,  his  legs  swelled,  and  he  was  obliged  to  apply  for  admission  to 
the  Infirmary.  The  cardiac  murmur,  for  such  it  proved  to  be,  continued 
auto-audible  for  a  few  weeks,  and  could  be  heard  at  a  distance  of  two 
feet  from  his  body  by  bystanders  ;  it  then  ceased,  and  he  has  not  heard 
it  since. 

On  examination,  cardiac  dropsy  and  the  other  signs  of  systemic  venous 
engorgement  were  present  ;  the  apex  beat  was  in  the  sixth  interspace, 
two  inches  below  the  left  nipple  ;  the  superficial  vessels  presented  the 
characteristic  Corrigan  pulsation  of  aortic  incompetence  ;  the  area  of 
prsecordial  dulness  was  much  increased  ;  a  faint  systolic  thrill  could  be 
felt  in  the  third  left  interspace  just  outside  the  sternum  ;  a  double 
bellows  murmur  was  loudly  heard  at  the  base  of  the  heart,  the  diastolic 
portion  of  the  murmur  was  propagated  over  the  course  of  the  aorta  and 
down  the  sternum  ;  at  the  lower  end  of  that  bone  it  was  loudly  heard  ;  it 
could  also  be  heard,  but  only  indistinctly,  at  the  cardiac  apex.  An  inde- 
pendent systolic  mitral  murmur  was  also  present.  There  was  extensive 
bronchitis. 

Under  digitalis  the  patient  greatly  improved,  and  was  made  an  out- 
patient on  November  27th. 

On  January  4th  he  was  re-admitted  veiy  much  worse  ;  and  he  died 
on  January  24th,  the  dropsy  and  orthopncea  having  rapidly  increased 
notwithstanding  the  free  administration  of  digitalis  and  other  remedies. 

On  post-mortem  examination  the  aortic  valve  was  found  to  be 
extremely  incompetent,  the  left  posterior  cusp  was  completely  ulcerated 
through,  a  nipple-like  process,  the  edges  of  which  were  perfectly  smooth 
(see  fig.  208)  being  all  that  remained  ;  the  surface  of  the  aorta  corre- 
sponding to  the  affected  valve  was  markedly  atheromatous,  the  adjacent 
portions  of  the  vessel  being  comparatively  healthy  ;  the  left  ventricle 
was  enormously  hypertrophied  and  dilated  ;  the  mitral  and  tricuspid 
orifices  dilated  ;  the  heart  weighed  45  ounces.  The  lungs  contained 
several  recent  patches  of  pulmonary  apoplexy  ;  there  was  great  subcu- 
taneous dropsy  and  considerable  effusion  into  all  the  serous  cavities. 

The  case  is  interesting  from  many  points  of  view  ;  but  space  does  not 
allow  me  to  go  into  details  further  than  to  say,  that  it  seems  completely 
to  disp.'ove  Dr  B.  Foster's  theor)',  that  when  the  left  posterior  valve 
segment  is  incompetent,  the  murmur,  instead  of  being  conducted  down 
the  sternum  is  propagated  towards  the  apex  of  the  heart.  The  great 
weight  of  the  heart  must  also  be  noted. 


3.  Acute  Endocarditis. — Aortic  incompetence  is  compara- 
tively rarely  established  during  the  acute  stage  of  simple 
endocarditis  ;  in    the  ulcerative  form   of  endocarditis  it  is  of 


Fig.  208.     Ulceration  of  one  of  the  Aortic  Cusps.    {Natural  size.") 

The  aortic  segment  corresponding  to  the  posterior  coronary  artery  is  completely  ulcerated 
through,  a  nipple-like  process  (a),  the  edges  of  which  are  perfectly  smooth  being  all  that  remains; 
the  sinus  of  Valsalva  corresponding  to  the  affected  cusp  is  dilated,  and  that  portion  of  the  aorta  (b), 
which  is  situated  above  the  affected  valve  is  atheromatous,  the  other  portions  of  the  vessel  (c), 
being  comparatively  healthy. 


Fig.  209.    Atheroma  of  the  base  of  the  Aorta:  Obstruction  of  the  orifices  of  the  Coronary  Arteries  ; 
Extreme  incompetence  of  the  Aoiiic  Valve.     (^Natural  size.) 

The  base  of  the  aorta  is  markedly  atheromatous,  and  contains  several  large,  flat,  smooth 
calcareous  plates ;  the  orifice  of  one  of  the  coronary  arteries  (a),  is  completely  occluded,  while 
that  of  the  other  (6)  is  very  much  narrowed ;  the  segments  of  the  aortic  valve  are  thickened 
and  crumpled ;  the  valve  was  extremely  incompetent. 


^ 

^ 


^Etiology  and  Pathology  of  Aortic  Incompetence.    503 

frequent  occurrence.^  The  appearances  which  the  \alve  pre- 
sents in  cases  of  acute,  simple,  and  ulcerative  endocarditis, 
have  previously  been  fully  described.     (See  page  403.) 

4.  Chronic  Endocarditis. — This  is  a  very  common  cause  of 
aortic  incompetence.  I  need  not  again  detail  the  different 
causes  of  chronic  endocarditis,  but  I  may  say  that,  in  the 
majority  of  cases  of  aortic  incompetence  which  result  from 
chronic  endocarditis  (as  distinct  from  atheroma),  the  inflam- 
mation of  the  endocardium  is  either  rheumatic  or  the  direct 
result  of  strain.  In  all  the  large  centres  of  laborious  work, 
in  Leeds,  for  example,  as  Dr  Clifford  Allbutt  has  pointed 
out,  and  in  Newcastle,  as  I  know  from  personal  experience, 
cases  of  aortic  incompetence  are  frequently  met  with  in 
}'oung  men  who  follow  laborious  occupations,  necessitating 
sudden  and  great  variations  in  the  arterial  pressure,  and  who 
have  never  suffered  from  rheumatism,  syphilis,  gout,  or  the 
other  diseases  with  which  endocarditis  and  atheroma  are 
usually  associated.  In  cases  of  this  description  the  base  of 
the  aorta  is  usually  dilated  ;  the  regurgitation  is,  in  fact, 
usually  due  both  to  organic  changes  in  the  valve  segments 
and  to  relative  incompetence. 

The  alterations  which  are  produced  in  the  aortic  valves  by 
chronic  inflammation  are  various.  In  the  great  majority  of 
cases,  all  three  segments  are  involved,  though  in  many  cases 
the  different  segments  are  unequally  implicated.  The  valve 
segments  are  thickened  ;  they  are  often  of  a  cartilaginous 
consistenc}',  and  in  many  cases  infiltrated  with  calcareous 
deposits.  The  natural  elasticity  of  the  affected  segments  is 
impaired  or  altogether  destroyed.  The  thickening  more  par- 
ticularly involves  the  free  edges  of  the  flaps,  the  Innnlce  being 
in  man}'  cases  completely  obliterated.  In  many  cases,  the 
whole  of  the  affected  segment  is  contracted  and  shrunk  ;  in 
others,  the  free  margins  are  crumpled  and  turned  inwards 
towards  the   base   of  the  aorta   (see   figs.    209  and    210)  ;  in 

'  I  do  not  of  course  mean  to  say  that  aortic  regurgitation  the  result  of  ulcera- 
tive endocarditis  is  frequently  met  with  in  practice,  but  that,  when  the  endocardium 
is  attacked  by  the  ulcerative  form  of  endocarditis,  aortic  regurgitation  fre- 
quently occurs.     Cases  of  ulcerative  endocarditis  are  comparatively  rare. 


504  Diseases  of  the  Heart. 

others,  again,  the  free  edge  is  inverted  towards  the  ventricle. 
In  a  few  cases,  one  or  more  of  the  valve  segments  have 
appeared  to  me  to  be  more  voluminous  and  dilated  than 
natural.  In  many  cases  the  adjacent  segments  are  adherent 
at  their  edges,  and  masses  of  calcareous  vegetations  are  not 
unfrequently  found  at  the  points  of  adhesion.  It  occasionally 
happens,  that  the  partition  formed  by  this  process  of  adhesion 
between  two  adjacent  flaps  breaks  down  and  gives  way,  two 
adjacent  pouches  being,  as  it  were,  thrown  into  one. 

5.  AtJicroina. — Atheromatous  changes  at  the  base  of  the 
aorta  are  very  frequently  associated  with  aortic  incompetence  ; 
in  some  cases  the  valvular  lesion  is  identical  with  that  which 
is  produced  by  chronic  endocarditis  (chronic  rheumatic  endo- 
carditis) ;  cases  of  this  description  may  occur  in  young  sub- 
jects, the  valvular  lesion  and  the  atheroma  usually  depending 
upon  a  common  cause,  viz.,  strain  ;  in  other  cases,  and  these 
are  more  apt  to  occur  in  old  people,  the  valvular  lesion  is 
rather  degenerative  than  inflammatory  in  character,  the  valve 
segments  being  calcified,  but  their  form  being  comparativel}^ 
little  interfered  with.  (Atheroma  of  the  root  of  the  aorta 
does  not  necessarily  produce  disease  of  the  aortic  valves. 
Cases  are  occasionally  met  with,  in  which  the  whole  base  is 
extremely  atheromatous,  but  in  which  the  valve  segments 
are  perfectly  natural  and  elastic.)  In  the  atheromatous 
disease  of  the  aortic  segments  which  occurs  in  old  people, 
marked  stenosis  is  often  combined  with  regurgitation  ;  and 
in  all  cases  of  aortic  incompetence,  in  which  the  regurgita- 
tion depends  upon  organic  changes  in  the  valve  segments, 
some  stenosis  may  be  present.  In  many  cases  of  aortic  in- 
competence, recent  vegetations  and  coagula  are  found  on  the 
affected  segments,  chronic  disease  of  the  valve  segments 
being,  as  we  have  previously  seen,  a  powerful  predisposing 
cause  of  recent  endocarditis. 

Method  of  testing  tJic  aortic  valve  after  death. — The  heart  is 
to  be  removed  in  the  usual  manner,  the  aorta  and  pulmonary 
artery  being  divided  about  two  inches  above  their  valvular 
orifices.  The  cavity  of  the  left  ventricle  must  then  be  opened, 
care  being  taken  to  avoid  division  of  any  of  the  larger  branches 


Pathology  of  Aortic  Incompetence.  505 

of  the  coronary  artery.  Any  clots  in  the  ventricular  cavit}-, 
and  especially  any  clots  which  are  sticking  in  the  aortic  orifice 
must  then  be  gcntl}-  removed  with  the  finger,  and  a  stream  of 
water  allowed  to  flow  from  above  into  the  aorta  and  pulmon- 
ary artery.  If  the  valve  holds  water,  it  is,  of  course,  quite 
competent.  It  must,  however,  be  remembered,  that  it  is 
difficult  to  fulfil  all  the  conditions  which  are  present  during 
life,  more  especially  the  forcible  distention  of  the  base  of  the 
aorta  ;  hence  it  is  that  in  some  cases  in  which  the  val\-e 
seemed  perfectly  healthy  during  life,  water  slowly  makes  its 
way  through  into  the  ventricle  after  death. 

Iiicoinpctcnce  due  to  dilatation  of  the  base  of  the  aorta,  the 
valve  segments  being  healthy.  Relative  incompetence  of  the 
aortic  valve  is  rare,  but  that  it  does  sometimes  occur  I  am 
perfectly  satisfied  from  cases  which  have  come  under  my  own 
personal  observation.  I  have  seen  several  cases  in  which 
the  base  of  the  aorta  was  dilated  (either  a  uniform  dilatation 
due  to  strain  and  associated  with  atheroma,  or  localised 
(aneurismal)  dilatation  immediately  above  the  valves),  the 
valve  segments  quite  healthy,  but  the  valve  incompetent  to 
the  water  test  after  death,  and  in  which  there  were  all  the 
usual  characteristic  signs  of  aortic  regurgitation  during  life. 

Pathological  Physiology. — -The  first  effect  of  aortic  regurgi- 
tation is,  of  course,  to  allow  some  of  the  blood  which  ought  to 
be  retained  in  the  aorta  to  flow  back  into  the  cavity  of  the  left 
ventricle  ;  in  other  words,  to  produce  ansemia  in  the  arterial 
system,  and  more  or  less  engorgement  behind  the  valvular 
orifice,  i.e.  in  the  cavity  of  the  left  ventricle  ;  so  long  as  the 
mitral  valve  is  competent,  the  circulation  behind  the  mitral 
orifice  is  very  little  interfered  with. 

The  second  effect  is  to  produce  a  series  of  changes  in  the 
heart  and  circulation,  which  are  briefly  as  follows  : — 

Effect  on  the  heart. — In  aortic  regurgitation  the  cavity  of 
the  left  ventricle  receives  blood  from  two  sources,  viz.,  the 
aorta  and  the  left  auricle  ;  it  is  therefore  more  rapidly  and 
more  fully  distended  than  in  health.  In  consequence  of  the 
forcible  distention  of  its  flaccid  walls  dilatation  is  produced 


5o6  Diseases  of  the  Heart. 

(see  figs.  I/I  and  210),  while  its  muscular  wall  is,  by  reason 
of  the  rapidity  with  which  the  cavity  is  filled,  more  rapidly 
stimulated  than  in  health,  and  the  frequency  of  the  cardiac 
contractio7is  is  increased.  The  increased  effort  which  is  re- 
quired to  expel  the  extra  quantity  of  blood  which  the  cavity 
contains  leads  also  to  the  production  of  hypertrophy} 

Now  all  of  these  changes — dilatation  and  hypertrophy  of 
the  ventricle,  and  increased  rapidity  of  the  cardiac  contractions 
— arc  within  certain  limits  beneficial  and  salutary.  When, 
for  example,  the  dilatation  is  just  sufficient  to  accommodate 
the  quantity  of  blood  which  regurgitates  from  the  aorta,  and 
at  the  same  time  to  receive  the  normal  quantity  of  blood  from 
the  left  auricle,  and  when  the  hypertrophy  is  sufficiently  great 
to  enable  the  cavity  to  be  completely  emptied  at  each  systole, 
the  compensation  is  perfect.  Under  such  circumstances  the 
circulation  behind  the  mitral  valve  is  little  if  at  all  interfered 
with  ;  and  provided  that  the  anaemia  in  the  arterial  system, 
which  necessarih'  occurs  during  the  ventricular  diastole  {i.e. 
in  consequence  of  the  regurgitation  of  some  of  the  blood  which 
ought  to  be  strained  in  the  arterial  system  into  the  left  ven- 
tricle) is  not  great,  and  provided  that  disastrous  consequences 
are  not  produced  in  the  peripheral  arteries  as  the  result  of 
their  excessive  distention  during  the  ventricular  systole,  there 
are  few,  if  any,  symptoms. 

In  many  cases  of  aortic  regurgitation  in  which  the  leak  is 
a  slight  one,  in  which  the  valvular  lesion  is  stationary,  and  in 
which  the  heart  and  organism  as  a  whole  are  healthy,  satisfac- 
tory compensation  is  maintained  for  years,  the  patient  being 
able  to  lead  a  comfortable  and  active  existence. 

In  other  cases  in  which  the  leak  is  greater,  and  more  espe- 
cially in  those  cases  in  which  the  valvular  lesion  is  progressive, 

'  The  heart  is  heavier  in  aortic  regurgitation  than  in  any  other  condition.  Dr 
Hilton  Fagge  has  recorded  a  case  in  which  it  weighed  48  ounces,  and  I  myself 
have  met  with  a  heart  weighing  45  ounces.  (See  case  p.  501.)  It  is  important 
to  observe,  as  was  first  pointed  out  by  Traube  (quoted  by  Rosenstein  in 
Zietnssen^s  Cyclopaedia,  vol.  vi.  p.  134),  '  that  the  papillary  muscles  are  not 
proportionately  enlarged  with  the  other  parts  of  the  left  ventricle — that  is,  they 
are  not  round  and  hypertrophied,  but  generally  lengthened  and  flattened,  cor- 
responding to  the  considerable  strain  to  which  they  are  exposed  during  diastole.' 


Pathology  of  Aortic  Incoiupetcnce.  507 

or  in  which  the  heart  and  organism  as  a  whole  are  in  an  un- 
healthy condition,  the  compensation  which  for  a  time  perhaps 
was  sufficient  to  balance  the  lesion  ultimately  gives  way  and 
disastrous  consequences  result.  In  cases  of  this  description, 
dilatation  gradually  gains  the  upper  hand,  and  the  arterial 
anaemia  becomes  excessive.  In  consequence  of  the  dilatation 
of  the  ventricle,  various  important  results  may  ensue  ;  in 
some  cases,  the  degenerated  and  weakened  muscle  is  para- 
lysed, as  it  were,  by  the  over-distention  of  the  cavity,  the 
heart's  action  is  arrested  in  diastole,  and  the  patient  suddenly 
drops  dead  ;  in  others,  the  dilatation  leads  to  relative  incom- 
petence of  the  mitral  orifice  ;  in  others  again,  the  nutrition  of 
the  ventricle  fails,  and  a  condition  of  asystole  is  gradually 
established. 

Effect  on  the  left  auricle,  pulmonary  circulation,  right  heart, 
and  systemic  venous  circulation. — In  the  earlier  stages  of  aortic 
regurgitation,  and  throughout  those  cases  in  which  compensa- 
tion remains  perfect,  there  is  little  or  no  interference  with  the 
free  passage  of  the  blood  from  the  cavity  of  the  left  auricle  ; 
the  engorgement  of  the  pulmonary  and  systemic  circulation  is 
so  slight  that  it  leads  to  no  practical  consequences.  In  the 
later  stages,  when  dilatation  is  in  excess  of  hypertrophy,  or 
when  relative  incompetence  of  the  mitral  valve  is  established, 
the  pulmonary  and  systemic  circulations  may  become  seri- 
ously embarrassed  ;  and  the  secondary  consequences  which  I 
have  previously  described  in  detail,  may  of  course  become 
established.^  Mitral  regurgitation  due  to  organic  changes  in 
the  valve  segments  is  not  unfrequently  associated  with  aortic 
regurgitation,  the  same  pathological  process  (chronic  endocar- 
ditis or  atheroma)  which  produces  the  aortic  lesion  having 
simultaneously  attacked,  or  subsequently  extended  to,  the 
anterior  segment  of  the  mitral  valve,  which  is  continuous  with 
the  posterior  aortic  segments.     (See  figs.  177  and  181.) 

Effects  on  the  arterial  circulation. — The  effects  which  aortic 
incompetence   produces  on  the   arterial  circulation   are  very 

'  Relative  incompetence  would  probably  be  of  more  freqnent  occurrence  if  it 
were  not  for  the  fact  that  in  many  cases  of  aortic  mcompetence  the  basal  ring  of 
the  mitral  valve  is  rigid  in  consequence  of  atheromatous  changes. 


5o8  Diseases  of  tJic  Heart. 

striking.  In  consequence  of  the  h\-pertrophicd  and  dilated 
condition  of  the  left  ventricle,  the  arterial  system  is  very  for- 
cibly and  very  fully  distended  during  the  ventricular  systole ;  as 
a  result  of  the  excessive  strain,  atheroma  is  apt  to  be  produced 
and  arterial  rupture  to  occur.  In  consequence  of  the  regurgita- 
tion, the  blood  pressure  in  the  aorta  and  arteries  generally, 
suddenly  falls  with  the  occurrence  of  the  ventricular  diastole, 
and  a  condition  of  peripheral  anaemia,  the  extent  of  which 
varies  of  course  with  the  extent  of  the  regurgitation,  remains 
until  the  occurrence  of  the  next  ventricular  systole.  It  will  now 
be  readily  understood  that  the  increased  frequency  of  the  car- 
diac contractions,  which  I  have  alrcad}'  alluded  to,  is  distinctly 
beneficial  and  compensatory,  for  not  only  does  the  contraction 
of  the  ventricle  arrest  the  reflux,  but  it,  at  the  same  time,  distends 
the  arteries,  and  is,  therefore,  in  a  twofold  manner  beneficial. 

The  effect  which  aortic  regurgitation  produces  on  the 
coronary  circulation,  i.e.  on  the  nutritive  supply  of  the  heart 
itself,  is  a  subject  of  much  importance,  and  has  given  rise  to 
considerable  debate.  It  was  formerly  supposed  that  during 
the  ventricular  systole  the  mouths  of  the  coronary  arteries 
were  covered  up  by  the  flaps  of  the  aortic  valve,  and  that  the 
blood  was  pumped  into  these  vessels  by  the  elastic  recoil  of 
the  aorta,  during  the  diastole  of  the  heart.  It  was  therefore 
supposed,  that  in  aortic  incompetence  the  distention  of  the 
coronary  arteries  would  be  imperfect,  and  the  nutrition  of  the 
heart  seriously  impaired.  Thanks  to  the  observations  of 
Martin  and  Sedgwick,  we  now  know  that  the  coronary 
arteries  are  distended  like  all  the  other  arteries  of  the  body 
during  the  ventricular  systole  ;  while  the  fact  that  the  left 
ventricle  is  able  to  become  so  enormously  hypertrophied  as  it 
does  in  many  cases  of  aortic  incompetence,  seems  to  show 
that  the  supply  of  blood  to  the  heart  is,  in  most  cases,  amply 
sufficient.  Nevertheless  it  must,  I  think,  be  conceded  that 
free  aortic  regurgitation  must  materially  interfere  with  the 
passage  of  the  blood  into  the  coronary  arteries  during  the 
ventricular  diastole.  We  may  further  suppose  that  this  in- 
terference will  be  greatest  when  the  coronary  segments  of  the 
valve  are  ruptured,  or  extensively  destroyed  by  disease. 


Clinical  History  of  Aortic  Incompetence.        509 

Clinicat  history. — The  symptoms  met  with  in  cases  of 
aortic  incompetence  are  more  intelHgible  when  it  is  remem- 
bered— 

1.  That  the  arterial  system  is  suddenly  and  widely 
distended  by  the  large  quantity  of  blood  which  is  pumped 
into  it  by  the  hypertrophied  and  dilated  left  ventricle. 

2.  That  on  the  cessation  of  the  ventricular  systole,  a  sudden 
collapse  in  the  arterial  tension  occurs,  and  the  arteries  are 
rapidly  emptied  during  the  ventricular  diastole. 

3.  That  in  all  cases  of  aortic  incompetence,  there  is  a 
tendency  to  sudden  over-distention  and  paralysis  of  the  left 
\'entricle. 

4.  That  in  a  considerable  number  of  cases  the  peripheral 
arteries  are  atheromatous  ;  that  in  others  the  thoracic  aorta 
is  dilated  or  is  in  an  aneurismal  condition  ;  while  in  others,  the 
sensory  nerve  fibres  which  ramify  so  abundantly  on  the 
outer  surface  of  the  aorta,  are  liable  to  be  irritated  and  im- 
plicated by  inflammatory  processes  originating  in  the  interior 
of  the  vessel. 

The  onset  is,  as  a  rule,  slow  and  insidious  ;  in  exceptional 
cases,  as,  for  example,  when  the  \alve  flaps  are  rapidly  de- 
stroyed by  ulceration,  or  ruptured  as  the  result  of  traumatic 
injury  or  excessive  strain,  urgent  symptoms  may  be  quick!}' 
or  suddenly  developed. 

Chronic  cases,  which  we  have  now  more  particularly  to 
consider,  may,  for  practical  and  teaching  purposes,  be  con- 
veniently di\'ided  into  two  groups  :  — 

I.  Cases  in  i^'hich  the  lesion  is  a  stationary  one,  and  in  zehieli 
the  regnrgitation  is  slight,  and  insnfficient  to  prodnce  any  eon- 
siderable  alteration  in  the  eoJidition  of  the  left  ventricle  or  in 
the  peripheral  arterial  circulation. 

In  cases  of  this  description  there  are  practically  no 
symptoms.  The  patient  may  perhaps  be  a  little  paler  than 
natural,  he  may  be  more  easily  fatigued,  and  unequal  to  pro- 
longed mental  effort  or  bodily  exertion,  but  nevertheless  able 
to  go  through  a  large  amount  of  mental  work,  and  to  enjoy 
life,  and  capable  of  active  exercise.  All  physicians  of  large 
experience   are   probably   acquainted    with   professional   men 


5IO  Diseases  of  tJie  Heart. 

who  have  for  years  been  the  subjects  of  aortic  incompetence  ; 
to  the  eye  of  a  layman  they  may  appear  to  be  perfectly 
healthy,  but  the  skilled  observer  can  usually  detect  evidence 
of  their  disease  in  the  pallor  of  the  face  and  the  jerking 
pulsation  in  the  carotids  and  more  particularly  in  the  peri- 
pheral vessels.  The  duration  of  these  cases  is  usually  long 
(ro,  20,  30  years  or  more).  It  must,  however,  be  remembered 
that  there  is  always  a  risk  of  the  lesion  increasing,  of  the 
failure  of  compensation,  and  of  the  occurrence  of  sudden 
death  from  temporary  over-distention  and  paralysis  of  the  left 
A-entricle. 

2.  Cases  in  which  the  lesioti  is  more  extensive,  and  in  wliich 
considerable  alterations  in  the  condition  of  the  left  ventricle,  and 
in  the  peripheral  aj'terial  cii'cnlation  are  produced. 

So  long  as  the  compensation  is  fairly  good  the  symptoms 
are  not  prominent.  The  face  is  pale,  and  usually  has  a  some- 
what anxious  expression.  Although  the  patient  can,  as  a  rule, 
take  a  considerable  amount  of  active  exercise  without  feeling 
short  of  breath,  there  is  a  loss  of  nerve  tone  and  of  muscular 
power  and  endurance ;  pains  in  the  back  and  lower  ex- 
tremities, such  as  result  from  nervous  exhaustion  are  some- 
times observed,  and  in  more  than  one  case  twitchings  in  the 
lower  extremites,  not  unlike  the  fibrillary  twitching  of  progres- 
sive muscular  atrophy,  have  come  under  my  notice.  These 
symptoms  depend,  I  think,  upon  anaemia  of  the  lumbar  en- 
largement of  the  spinal  cord.  Twitchings  in  the  facial  muscles 
may  also  occur.  In  one  case  which  came  under  my  observa- 
tion some  years  ago,  twitchings  in  the  facial  and  labial 
muscles,  slowness  in  cerebration,  and  thickness  and  hesitation 
in  labial  speech,  all  seemed  to  depend  upon  cerebral  anaemia, 
the  result  of  very  free  aortic  regurgitation,  and  gave  the  case  a 
close  resemblance  to  general  paralysis  of  the  insane.  Noises 
in  the  ears,  flashes  of  light  before  the  eyes,  throbbings  of  the 
peripheral  blood  vessels,  headache,  giddiness  or  actual  fainting, 
and  many  other  symptoms  (due  either  to  sudden  distention  of 
the  arterial  system  during  the  cardiac  systole,  or  to  anaemia 
during  diastole)  are  of  common  occurrence.  Palpitation  is 
frequentl}'  complained  of.     Pain   in  the  region  of  the  heart, 


Symptoins  of  Aortic  Inconipetcnce.  51 1 

and  in  some  cases  attacks  of  true  angina  pectoris  are  not  very 
uncommon  ;  these  symptoms  depend,  I  think,  in  some  cases 
upon  over-distention  and  spasm  of  the  ventricular  wall,  in 
others  upon  irritation  of  the  branches  of  the  cardiac  plexus  of 
nerves. 

When  the  compensation  begins  to  fail,  all  of  these  symp- 
toms become  more  prominent,  and  the  patient  now,  perhaps, 
for  the  first  time,  is  actually  short  of  breath.  The  arterial 
anaemia  during  diastole  and  the  shortness  of  breath  gradually 
increase.  Dropsy  and  pulmonary  complications  may  now 
develop,  and  usually  show  that  the  mitral  valve  has  become 
incompetent.  The  symptoms,  in  fact,  in  the  terminal  stage  of 
aortic  regurgitation  are  partly  due  to  engorgement  of  the 
pulmonary  and  systemic  venous  circulations,  the  result  of 
mitral  regurgitation,  and  partly  to  arterial  anaemia,  the  result 
of  the  primary  {i.e.  the  aortic)  lesion. 

Embolic  symptoms,  caused  by  particles  of  fibrine  which 
have  become  detached  from  the  aortic  segments  and  carried 
to  distant  parts  of  the  circulation,  may  occur  at  any  stage  of 
the  case.  In  cases  of  this  description,  acute  or  sub-acute  in- 
flammatory changes  are  usually  present  in  addition  to  the 
chronic  lesion,  and  it  is  in  consequence  of  these  more  active 
changes  that  the  fibrine  is  deposited  on  the  aortic  segments. 
When  the  aorta  is  much  dilated  or  in  an  aneurismal  condition, 
other  symptoms,  which  I  shall  afterwards  describe  in  treating 
of  aneurisms  may  be  present.  When  the  arteries  are  exten- 
sively atherosed,  apoplexy  and  other  complications  may  arise. 

The  duration  of  cases  of  aortic  regurgitation  included 
under  this  group  is  very  variable.  Once  compensation  begins 
to  fail,  the  downward  progress  is  usually  rapid.  Death  may 
occur  at  any  stage  from  sudden  failure  of  the  action  of  the 
left  ventricle. 

Physical  signs. — A  diastolic  murmur,  having  its  point  of 
differential  maximum  intensity  at  the  base  of  the  heart,  or 
(in  some  cases)  at  the  lower  end  of  the  sternum,  heard  at  the 
aortic  cartilage  and  propagated  downwards  along  the  sternum 
or  towards  the  apex  of  the  heart  (see  fig.  21 1).  is  characteristic 


5  1  2  Diseases  of  iJie  Heart. 

of  aortic  regurgitation.  The  murmur  is  usually  soft  and 
blowing  ;  in  some  cases  it  is  very  faint,  in  others  loud  antl 
(occasionally  though  rarely)  musical.  A  systolic  aortic  mur- 
mur, which  is  usually  due  to  associated  stenosis  of  the  aortic 
orifice,  but  which  may  be  caused  by  dilatation  of  the  ascending 
thoracic  aorta,  or  possibly  b\'  anxmia,  is  frequent!}^  also  pre- 
sent. 


Flo.  211. — Outline  figure  showing  jjoint  of  differential  maximum  intensity  (*) 
(if  the  diastolic  murmur  (aortic  regurgitation);  and  the  directiun  in  which  it  is 
propagated. 

In  some  cases  the  second  sound  is  completely  replaced 
by  the  murmur  ;  in  others,  both  the  second  sound  and  the 
murmur  are  audible.  Occasionally  the  second  sound,  which 
is  totally  obscured  at  the  base  of  the  heart,  can  be  heard  in 
the  carotid  artery.     (Rosenstein.)  ^ 

A  diastolic  thrill  may  sometimes  (though  rarelyj  be  felt 
when  the  hand  is  placed  over  the  base  of  the  heart.  (A 
systolic  thrill  is  jjresent  in  many  of  the  cases  in  which  a 
double — systolic  and  diastolic — aortic  murmur  is  audible.) 

'^  Ziemsseii's  C)clopadia  of  Medici  i^e,  vol.  vi.  p.   136. 


PJivsical  Signs  of  Aortic  Incompetence.        513 

In  addition  to  the  diastolic  murmur  and  diastolic  thrill, 
which  we  may  term  the  primary  physical  signs  of  aortic 
incompetence,  others,  due  to  secondary  changes  in  the  left 
\-entricle  and  the  altered  condition  of  the  arterial  circulation, 
are  present.  The  more  important  of  these  secondary  physical 
signs  are  : — 

1.  Displacement  of  the  apex  downwards  and  outwards. 

2.  Increase  of  the  cardiac  dulness. 

3.  A  powerful  heaving  action  of  the  heart. — (This  con- 
dition which  depends  upon  hypertrophy  of  the  left  ventricle, 
may  not  be  present  in  the  later  stages  of  the  case,  i.e.  when 
dilatation  is  in  excess  of  hypertrophy.) 

4.  Alterations  in  the  character  of  the  arterial  pulse. — 
The  sudden  distention  of  the  arterial  system  which  results 
from  the  large  quantity  of  blood  which  is  propelled  into  the 
aorta  by  the  dilated  and  hypertrophied  left  ventricle,  and  the 
sudden  collapse  which  occurs  as  the  result  of  the  back  flow 
into  the  left  ventricle  during  the  ventricular  diastole,  produce 
very  striking  alterations  in  the  carotid,  radial,  and  other  peri- 
pheral pulses. 

The  pulse  is  quicker  than  normal  ;  as  a  rule  it  is  quite 
regular  ;  the  distention  of  the  artery  is  sudden  and  the  pulse 
is  jerking,  visible,  collapsing,  and  tortuous  ;  it  has  been  called 
the  water-hammer  pulse,  or  Corrigan's  pulse  (after  Sir  Dominic 
Corrigan,  who  first  described  these  features).  The  jerking, 
visible  and  collapsing  characters,  are  usualh^  made  more  pro- 
minent by  raising  the  arm  abo\'e  the  head.  It  must,  howexer, 
be  remembered  that  when  the  heart  is  acting  ver)'  feebl\-, 
raising  the  arm  may  make  the  pulse  less,  rather  than  more 
visible.  A  sphj^gmographic  tracing  shows  that  the  artery  is 
o\'er-distended  during  the  ventricular  systole,  and  under- 
distended  during  the  ventricular  diastole.  The  aortic  wave 
is  situated  low  down  in  the  tracing,  and  is  usually,  but  not 
invariabl)',  less  prominent  than  in  health  ;  in  some  cases  it 
is  altogether  effaced.     (See  figs.  212  and  213.) 

A  systolic  murmur,  which  is  probably  due  to  \ibrations 
produced  in  the  arterial  coats  by  the  rapid  distention  during 
the  ventricular  .systole,  can   often   be  heard   in  the  peripheral 

K  K 


514  Diseases  of  the  I  I  earl. 

vessels.     When  the  regurgitation  is  free,  a  diastolic  murnuir 
can  also  be  heard  in  the  peripheral  arteries.     When  the  arte- 


Yxi:,.  2\2.  — Pressure  2h  oz.  Y \(\.  213.  —  Pressitre  t,  oz. 

Figs.  212  and  213. — Pulse  tracings  in  a  case  of  Aortic  Regurgitation. 

The  tracing  shown  in  fig.  212  was  taken  on  the  patient's  admission  to  hospital  ; 
the  arteries  were  almost  empty  during  the  ventricular  diastole.  (2-^=up-stroke  ; 
ii=apex  ;  f  =  tidal  wave;  d  indicates  the  position  of  the  aortic  wave,  which  is 
absent  in  this  tracing. 

Fig.  213. — Taken  from  the  same  patient  after  the  administration  of  iligitalis. 
The  letters  have  the  same  significance  as  in  fig.  212. 

rial  walls  are  atheromatous,  when  the  mitral  valve  is  incom- 
petent, and  when  the  heart  is  very  feeble,  the  characters  of  the 
pulse,  which  I  have  just  described,  may  become  variously 
modified. 

5.  Capillary  and  venous  pulse. — In  aortic  regurgitation  a 
pulse  wave  can  sometimes  be  seen  in  small  vessels,  such,  for 
example,  as  the  retinal  vessels  and  the  capillaries  of  the 
skin,  in  which,  under  normal  circumstances,  pulsation  is  in- 
visible. The  capillary  pulsation  in  the  skin  is  best  elicited 
by  drawing  the  finger  over  the  skin  (the  skin  of  the  forehead, 
for  example),  and  producing  a  capillary  blush,  which  is  seen 
to  expand  and  retract,  i.e.  to  pulsate,  with  each  ventricular 
systole.  The  capillary  pulse  is  doubtless  due  to  the  fact 
that  the  large  blood  wave  which  is  propelled  with  abnormal 
suddenness  and  force,  by  the  dilated  and  hypertrophied  left 
ventricle  into  the  relaxed  arteries,  makes  its  way  as  a  ptilse  or 
wave  into  vessels  into  which,  under  normal  cirumstances,  the 
pulse  wave  does  not  penetrate. 

A  venous  pulse,  .synchronous  with  the  systole  of  the  left 
ventricle,  is  occasionally  seen  in  the  peripheral  veins  (the  veins 
on  the  back  of  the  hand  for  example) ;  it  owes  its  origin  to 
the  same  cause,  viz.,  the  pulse  wave  passing  on  right  through 
the  capillaries  into  the  venous  circulation. 


Physical  Signs  of  Aortic  luconipttencc.        51 


The  capillary  and  venous  pulses,  which  depend  on  the 
force  with  which  the  blood  is  propelled  into  the  relaxed 
arteries,  disappear  when  dilatation  becomes  excessive,  i.e.  on 
the  failure  of  compensation. 

Should  the  mitral  valve  give  way,  the  usual  primary  and 
secondary  physical  signs  indicative  of  that  condition  will 
of  course  be  present ;  the  pulse  then  loses  some  of  these 
characteristics,  though  it  usually  still  presents  the  suddenness 
of  rise  and  rapidness  of  fall  which  it  has  in  the  earlier  stages 
of  the  case. 

6.  Alterations  in  the  character  of  the  cardiographic  tracing. 
— The  character  of  the  cardiographic  tracing  depends  upon 
{a)  the  condition  of  the  left  ventricle  (whether  hypertrophy 
or  dilatation  is  in  excess),  and  [b)  the  extent  of  the  incom- 
petence. The  most  characteristic  alteration  is  the  short  dura- 
tion of  the  diastolic  portion  of  the  tracing  and  the  rapid  filling 
of  the  ventricle  during  its  diastole — alterations  which  are  still 
more  marked  when,  in  addition  to  the  aortic  incompetence, 
mitral  regurgitation  is  present. 


Fig.  214.  Fig   215. 

Fig.  214. —  Cardioi^ra/ii  from  a  case  of  aortic  rc'^iirgitaliou. — [After  Galabin.) 
'Thomas  -S.,  Kt.  45.     The  diastolic  murmur  was  very  loud  and  accompanied 
by  a  thrill  felt  at  the  apex,  P.  74.'—  {Guys  Hospital  Reports,  1875,  p.  313.) 

Fig.  215.—  Cardiogram  in  a  case  of  aortic  regurgitation.  —  [After  Ga/abin.) 
'  The  heart  was  much  dilated,  the  apex  beat  being  in  the  sixth  intercostal  space, 
and  external  to  the  line  of  the  nipple.  The  pulse  tracing  showed  extreme 
collapse  in  the  diastolic  portion,  and  an  almost  entire  absence  of  the  tidal  wave. 
From  this  it  may  be  inferred  that  the  regurgitation  was  very  free,  and  the  contrac- 
tions of  the  heart  short  and  incomplete.  The  tracing  is  partly  inverted,  and  a 
retraction  occurs  during  the  latter  part  of  systole,  followed  by  a  sudden  recoil." 
— [Gufs  Hospital  Reports,  1875,  p.  312.) 


5  1 6  Ihseast's  of  I  he  FIcart. 

When  hypertrophy  is  in  excess  of  dilatation  the  summit  of 
the  systoUc  portion  of  the  tracing  may  be  broad  ;  when  dila- 
tation has  gained  the  upper  hand,  the  summit  of  the  systolic 
portion  of  the  tracing  is  pointed,  and  the  subsequent  descent 
of  the  lever  rapid.     (Sec  figs.  214  and  215.) 

In  some  cases,  as  in  figure  215,  the  presence  of  the  murmur 
or  thrill  is  demonstrated  in  the  diastolic  portion  of  the  tracing 
by  a  series  of  indentations  or  serrated  curves. 

Diagnosis. — When  a  case  of  supposed  aortic  regurgita- 
tion comes  under  notice  we  have  to  determine  : — 

(1)  Is  aortic  regurgitation  actually  present  .^ 

(2)  If  aortic  regurgitation  is  present,  is  it  due  to  disease 
originating  in  the  endoca'-dium,  or  to  disease  originating  in 
the  aorta  .' 

(3)  What  is  the  extent  and  gravity  of  the  lesion  .' 

Step  Xo.  I. — Is  aortic  regurgitation  actually  present  ? — The 
solution  of  this  question  is  seldom  attended  with  any  dififi- 
cult}'.  The  characteristic  ph}'sical  sign  of  aortic  incompe- 
tence is,  as  we  have  previous!}-  seen,  a  diastolic  aortic 
murmur  ;  and  since  a  diastolic  murmur  may  (theoretically) 
be  generated  at  the  mitral,  tricuspid,  and  pulmonary  orifices, 
in  other  words,  as  the  result  of  mitral  stenosis,  tricuspid 
stenosis,  and  pulmonary  regurgitation,  an  inexperienced  ob- 
server might  suppose  that  the  condition  would  be  likely  to 
give  rise  to  difficult}'.  As  a  matter  of  fact,  mitral  stenosis 
does  occasionally  produce  a  diastolic  murmur,  but  this  mur- 
mur has  its  point  of  maximum  differential  intensity  in  the 
mitral  area,  and  can  be  readily  distinguished  from  a  diastolic 
murmur  indicative  of  aortic  regurgitation  b}-  attention  to  the 
other  points  which  ha\'e  been  prexiously  detailed  in  speaking 
of  the  differential  diagnosis  of  mitral  stenosis. 

Tricuspid  stenosis  is  comparati\ely  rare.  So  far  as  I  am 
aware,  a  diastolic  (as  distinguished  from  a  presystolic)  murmur 
has  not  been  observed  in  that  condition.  But  even  if  a 
diastolic  murmur  is  sometimes  present  in  tricuspid  stenosis, 
it  would  be  impossible  for  an  experienced  observer  to  mistake 


Diagnosis  of  Aortic  Incompetence.  5  i  7 

that  condition  for  aortic  regurgitation.  (This  point  will  be 
more  apparent  after  the  tricuspid  lesions  have  been  described.) 

A  diastolic  pulmonary  murmur  is  practically  unknown, — 
and  even  if  it  did  occur  the  secondary  alterations  in  the  heart 
and  circulation  are  so  totally  different  from  those  which  are 
produced  by  aortic  regurgitation  that  the  two  conditions  could 
not  be  confounded. 

A  more  practical  question  is  the  differential  diagnosis  of 
the  double  murmur  of  aortic  disease  and  the  double  murmur 
due  to  pericarditis  ;  but  since  this  point  has  been  previously 
considered  in  detail  (see  p.  328),  I  need  not  recapitulate  the 
points  of  distinction  between  the  two  conditions. 

Step  No.  2. — If  aortic  regurgitation  is  present,  is  it  due  to 
disease  originating  in  the  endocardium  (i.e.  to  endocarditis),  or 
to  disease  originating  in  tlie  aorta  (i.e.  to  atlieronia,  aneurism, 
or  simple  dilatation  of  the  aorta,  etc.)  ? 

In  attempting  to  decide  this  question,  we  must  take  into 
consideration  the  following  points  : — 

(i)  The  age,  sex,  and  occupation  of  the  patient,  and  the 
previous  history  of  the  case. 

Youth,  the  female  sex,  the  fact  that  the  patient  has  not 
been  subjected  to  strain,  a  history  of  acute  rheumatism  or 
of  some  other  affection  in  the  course  of  which  endocarditis 
is  like  to  arise,  are  strongly  in  favour  of  the  endocardial 
origin  of  the  disease.  Vice  versa  when  the  patient  is  a 
male,  when  he  has  been  exposed  to  strain,  has  suffered  from 
syphilis,  or  indulged  in  alcoholic  excess,  when  there  is  no 
history  of  rheumatism  or  other  disease  likely  to  be  attended 
with  endocarditis,  and  more  particularly  when  he  is  advanced 
in  years,  the  aortic  or  arterial  origin  of  the  lesion  is  probable. 

(2)  The  condition  of  the  aortic  and  peripheral  vessels  as 
determined  by  physical  examination,  and  by  the  character  of 
the  symptoms  which  are  present. 

The  physical  signs  of  a  dilated  aorta  (see  page  696),  an 
atheromatous  condition  of  the  superficial  vessels,  and  the  pre- 
sence of  symptoms  indicative  of  intra-thoracic  pressure,  are 
strongly  in  favour  of  the  aortic  origin  of  the  lesion. 


1 8  Diseases  of  tlie  Heart. 


Pain  in  the  region  of  the  heart,  and  attacks  of  angina 
pectoris  (which  often  depend  upon  disease  of  the  coronary 
arteries,  and  therefore  upon  atheroma)  are  also  in  favour  of 
the  aortic  origin  of  the  lesion. 

Step  No.  3. —  What  is  the  extent  and  gravity  of  the  lesion  f 
This  question  will  be  more  appropriately  considered  under 
the  prognosis,  to  which  I  now  pass. 

The  Prognosis. — The  risk  of  sudden  death  is  very  much 
greater  in  aortic  regurgitation  than  in  any  other  form  of 
valvular  lesion.  Barring  this  risk  (which  may  be  considered 
as  accidental,  for  it  is  impossible  to  exclude  it  even  in  cases 
in  which  the  lesion  is  comparatively  slight,  and  it  of  course 
does  not  always  occur  even  in  severe  cases),  the  average  pro- 
spect of  life  duration  is  better  in  aortic  regurgitation  than  the 
average  prospect  in  mitral  lesions  ;  and  life,  so  long  as  it  lasts, 
is  infinitely  more  enjoyable. 

Individual  cases  must,  however,  be  judged  on  their  own 
merits  ;  and  in  trying  to  estimate  the  gravity  of  the  lesion  in 
any  individual  case  which  comes  before  us,  we  must  take  into 
consideration  the  following  points  : — 

(i)  The  extent  of  the  lesion. — This  is  estimated  by  (a)  the 
extent  and  character  of  the  secondary  changes  in  the  left 
ventricle,  {b)  the  degree  of  anaemia  in  the  arterial  system  during 
the  ventricular  diastole,  and  (c)  the  urgency  of  the  symptoms 
which  are  present.  The  greater  the  hypertrophy  and  dilata- 
tion of  the  left  ventricle,  the  greater  the  arterial  anaemia,  and 
the  more  urgent  the  symptoms  produced  by  the  anaemia,  such, 
for  example,  as  attacks  of  syncope-^the  greater  the  incom- 
petence. A  diastolic  murmur  in  the  peripheral  vessels,  a 
capillary  or  venous  pulse,  all  indicate  extensive  regurgitation.^ 

(2)  The  (etiology  of  the  ease. — The  extent  of  the  lesion 
being  equal,  aortic  incompetence  due  to  aortic  or  arterial 
change  is  a  more  serious  condition  than  aortic  incompetence 

'  I  presume,  of  course,  that  the  hypertrophy  and  other  cardiac  changes  are  due 
to  the  aortic  regurgitation,  and  not  to  other  conditions,  such  as  atheroma,  for 
example. 


Prognosis  of  Aortic  Incoiupeteiice.  519 

due  to  endocarditis.  When  the  regurgitation  is  due  to 
atheroma,  the  patient  is  older,  and  the  capabilities  of  compen- 
sation are  not  so  great ;  the  coronary  arteries  are  frequently 
involved  in  the  atheromatous  process,  and  the  nutrition  of  the 
heart  is  therefore  interfered  with  ;  the  risk  of  arterial  rupture 
(cerebral  apoplexy,  for  example)  is  very  considerable.  All  of 
these  circumstances  make  atheromatous  aortic  regurgitation 
(the  extent  of  the  lesion  being  the  same)  more  serious  than 
endocarditic  aortic  regurgitation.  A  dilated  condition  of  the 
aortic  arch,  and  especially  an  aneurismal,  as  distinct  from  a 
uniform  dilatation,  adds  seriously  to  the  dangers  of  the  case. 

Regurgitation  due  to  rupture  of  an  aortic  segment,  is  the 
most  serious  form  of  the  disease. 

(3)  The  capabilities  of  compensation. — The  same  general 
principles  which  have  been  laid  down  in  treating  of  the  prog- 
nosis of  mitral  lesions  apply  here.  It  must  however  be  re- 
membered, that  in  aortic  lesions  the  pulmonary,  digestive, 
excretory,  and  nervous  organs,  and  the  walls  of  the  heart 
itself,  are  protected  from  the  baneful  effects  of  venous  engorge- 
ment ;  so  long,  therefore,  as  the  mitral  valve  remains  com- 
petent, the  capabilities  of  compensation  are  much  greater  in 
aortic  than  in  mitral  cases. 

(4)  TJie  risk  of  accidents  and  complications. — Barrin  g  sudden 
death  and  accidental  complications  due  to  atheroma,  the  risk 
of  complications  is  much  less  in  aortic  than  in  mitral  cases. 

Treatment. — In  cases  of  aortic  regurgitation  due  to  rheu- 
matic valvulitis,  little  or  no  drug  treatment  is  required  so  long 
as  compensation  remains  good.  At  this  stage  of  the  case,  the 
general  rules,  which  have  been  recommended  for  the  treatment 
of  organic  mitral  regurgitation  previous  to  the  failure  of 
compensation  (see  page  467)  must  be  carried  out ;  the  main 
object  being  to  maintain,  the  tissues  as  a  whole,  and  the 
cardiac  muscle  in  particular,  in  the  highest  possible  state  of 
health.  Much  more  exercise  can  be  indulged  in  and  allowed 
than  in  cases  of  mitral  disease,  in  fact,  patients  affected  with 
this  form  of  aortic  incompetence  {i.e.  aortic  incompetence  the 
result  of  valvulitis  and  before  the   failure   of  compensation) 


520  Diseases  of  the  Heart. 

should  be  encouraged  to  lead  active  out-door  lives  ;  and  they 
may  engage  in  any  exercise  which  does  not  involve  strain  and 
which  does  not  over-tax  the  heart.  It  is  as  well  to  err  on  the 
side  of  caution,  for  unlike  the  subjects  of  mitral  incompetence 
patients  affected  with  aortic  incompetence  have  little  or  no 
shortness  of  breath,  and  experience  no  sensations  which  in- 
dicate the  limit  to  which  exertion  may  be  safely  carried. 
Violent  or  prolonged  exertion  should  be  avoided. 

The  tendency  to  sudden  death  from  syncope  and  over- 
distention  of  the  left  ventricle  must  be  remembered;  and 
patients  affected  with  this,  and  indeed  with  all  forms  of  aortic 
incompetence,  must  be  emphatically  told  to  avoid  everything 
likely  to  induce  syncope.  Excesses  of  all  kinds,  but  more 
especially  se.xual  excesses  and  over-indulgence  in  tobacco, 
are  to  be  prohibited  ;  strong  purgatives,  Turkish  baths  or 
prolonged  immersion  in  the  ordinary  warm  bath,  all  of  which 
tend  to  produce  fainting,  should  be  avoided.^ 

In  the  cases  in  which  the  aortic  incompetence  is  associated 
with  atheroma,  the  patient  should  lead  a  quiet  life;  in  cases  of 
this  description,  only  so  much  exercise  as  is  required  to  main- 
tain the  general  health  should  be  permitted  ;  everything,  such  as 
straining  at  stool,  sudden  effort,  etc.,  which  suddenly  increases 
the  arterial  blood  pressure,  and  which  is  therefore  apt  to  pro- 
duce rupture  of  the  degenerated  vessels,  is  to  be  avoided. 

In  those  cases  in  which  the  aortic  incompetence  is  asso- 
ciated with  aortic  aneurism,  iodide  of  potassium  and  the 
other  measures,  which  will  be  detailed  when  the  treatment  of 
aortic  aneurism  comes  under  consideration  (see  page  740), 
should  be  adopted.  (Iodide  of  potassium  is  often  very  useful 
in  those  cases  of  aortic  incompetence  which  result  from  in- 
creased arterial  tension,  and  in  which  there  is  no  aneurism.) 

When  the  left  ventricle  begins  to  fail,  and  dilatation  to  out- 
strip hypertroph)',  cardiac  tonics  and  stimulants  are  called  for. 

'  I  have  known  death  result  from  the  exhaustion  following  coitus,  in  a  patient 
affected  with  aortic  regurgitation.  In  another  case  the  patient  tumbled  down  in 
a  faint  after  a  copious  watery  evacuation  of  the  bowels  ;  such  an  accident  may  of 
course  occur  to  a  healthy  person,  but  is  much  more  likely  to  arise,  and  is 
dangerous,  in  a  person  affected  with  aortic  incompetence.  In  the  case  to  which 
I  refer,  the  syncope  was  recovered  from. 


Treatjiteui  of  Aortic  Inconipeteiice.  521 

Arsenic  is  the  remedy  which  has  seemed  to  me  most  useful 
in  the  earher  stages  of  this  affection  ;  iron  is  also  in  many 
cases  beneficial.  When  arsenic  and  iron  fail,  digitalis  or  some 
of  the  other  cardiac  tonics  should  be  given.  Marked  improve- 
ment generally  follows  the  administration  of  digitalis,  but  the 
remedy  should  be  cautiously  and  judiciously  administered,  for 
large  doses  are  not  so  well  borne  in  cases  of  aortic  incom- 
petence as  in  mitral  disease.  This  drug  should  not  be  in- 
discriminately prescribed  in  aortic  regurgitation;  and  when  its 
administration  is  necessitated,  the  dose  should  be  small  and 
the  remedy  should  be  discontinued  as  soon  as  the  required 
tonic  effect  has  been  produced.  If  these  points  be  attended 
to,  digitalis  will  often  be  found  pre-eminently  beneficial. 
Alcoholic  stimulants  are  often  useful,  but,  like  digitalis,  they 
must  be  judiciously  administered,  more  especially  in  those 
cases  in  which  the  aortic  incompetence  is  associated  with 
general   atheroma. 

For  the  relief  of  cardiac  pain,  which  is  of  frequent  occur- 
rence in  cases  of  aortic  incompetence,  more  especially  in 
atheromatous  cases,  arsenic  is  most  useful ;  the  application  of 
a  belladonna  plaster  to  the  praecordial  region  often  seems  to 
give  relief  When  attacks  of  genuine  angina  pectoris  occur, 
the  measures  which  will  be  afterwards  recommended  for  the 
treatment  of  that  condition  must  be  adopted.    (See  page  6^6^) 

AORTIC    STENOSIS. 
Dcji/iitioii. — Narrowing  of  the  aortic  orifice. 

yEtiology  and  Pathology. — Narrowing  of  the  aortic  orifice 
may  result  from  acute  endocarditis  with  the  formation  of 
luxuriant  vegetations,  or  from  chronic  endocarditic  or  athero- 
matous changes  in  the  valve.  The  stenosis  is,  in  the  majority 
of  cases,  combined  with  incompetence,  though  exceptions  to 
this,  the  general  rule,  are  occasionally  met  with,  generally  in 
old  people.  In  some  of  the  combined  cases  {i.e.  cases  of  aortic 
stenosis  and  aortic  incompetence),  stenosis  is  in  excess,  but  in 
the  majorit}^  the  regurgitant  lesion  is  the  more  important.  I 
need  not  farther  consider  the  latter  group  of  cases,  in  which 


522  Diseases  of  the  Heart. 

the  condition  practically  corresponds  in  most  cases  to  (pure) 
aortic  incompetence,^  but  will  limit  my  remarks  to  those  cases 
in  which  the  stenosis  is  the  only  or  the  predominant  lesion, 
and  in  which  the  lesion  is  a  chronic  one."  The  narrowing 
may  be  due  to  adhesion  of  the  valve  segments,  as  the  result 
of  inflammatory  changes  either  during  foetal  life  or  after  birth, 
and  sclerotic  and  atheromatous  changes  in  the  valve  segments 
and  basal  ring  of  the  aorta.  In  many  cases  these  two  pro- 
cesses (adhesion  of  the  segments  and  atheromatous  changes) 
are  combined. 

Aortic  stenosis  is,  in  its  pure  and  typical  form,  essentially 
a  disease  of  later  life,  and  is  usually  combined  with  general 
atheroma  and  calcification  of  the  arteries.  Fothergill  supposes 
that  '  when  the  valvulitis  tends  toward  aortic  stenosis,  the 
growth  commences  at  the  base  of  the  cusps,  and  from  thence 
spreads  towards  the  free  edges  ;  and,  synchronously,  there  is 
a  growth  of  connective  tissue  corpuscles  in  the  arterial  conus, 
so  that  there  is  stenosis  of  the  conus  along  with  obstruction 
due  to  the  stiffened  valve.  .  .  .  On  the  other  hand,  in 
young  subjects,  the  growth  commences  in  the  fibrous  structure 
of  the  free  edge  of  the  cusps,  extending  from  the  corpora 
Arantii  to  the  insertion  of  the  cusps  in  the  aortic  wall  ;  so 
that  the  free  edge  is  thickened,  and  then  in  time  contracted, 
consequently  the  cusps  become  insufficient,  and  there  is  regur- 
gitation through  them  on  the  aortic  recoil.'^ 

Pathological  Physiology. — The  first  effect  of  aortic  stenosis 
is  of  course  to  interfere  with  the  passage  of  the  blood  from 
the  cavity  of  the  left  ventricle  into  the  aorta  during  the  ven- 
tricular systole  ;  the  second  is  to  produce  a  series  of  changes  in 
the  heart  and  circulation,  which  are  as  follows  : — 

Effect  on  the  left  ventricle. — In  consequence  of  the  increased 
effort  which  is  required  to  force  the  blood  through  the  stenosed 
orifice,  the  left  ventricle  becomes  hypertrophied,  its  systole  is 
prolonged,  and  the  frequency  of  the  cardiac  contractions  is 

'   See  page  509. 

-'  The  acute  lesions  of  the  valves  are  described  on  p.  368. 

'  Diseases  of  the  Heart,  p.  159. 


Pathology  of  Aortic  Stenosis.  523 

diminished.  (In  those  cases  in  which  the  stenosis  is  accom- 
panied by  regurgitation,  the  cavity  of  the  left  ventricle  also 
becomes  dilated,  but  in  stenosis  per  se  there  is  little  or  no 
dilatation.)  Both  changes  (hypertrophy  of  the  left  ventricle 
and  prolongation  of  the  ventricular  systole)  are  beneficial  and 
compensatory,  inasmuch  as  they  allow  an  increased  quantity 
of  blood  to  pass  through  the  narrowed  orifice  at  each  ven- 
tricular systole. 

Effect  on  the  left  auricle,  pnluwnary  circulation,  right  heart 
and  systemic  venous  circulation. — So  long  as  the  hypertrophy 
of  the  left  ventricle  is  good  (and  in  pure  cases  of  aortic  sten- 
osis the  compensation  usually  remains  satisfactory  for  a  con- 
siderable, and  in  many  cases  for  a  long  time),  the  pulmonary 
and  systemic  venous  circulations  are  little  if  at  all  interfered 
with,  and  there  are  no  evident  indications  of  secondary 
changes  in  the  left  auricle  or  right  heart.  After  the  failure  of 
compensation,  and  when  the  cavity  of  the  left  ventricle  be- 
comes dilated,  the  pulmonary  and  venous  circulations  may 
become  engorged,  and  secondary  (relative)  mitral  incompetence 
may  occur. 

Effects  on  the  arterial  circulation. — The  amount  of  blood 
which  is  propelled  into  the  aorta  at  each  contraction  of  the 
left  ventricle  is,  in  cases  of  advanced  stenosis  of  the  aortic 
orifice,  smaller  than  normal,  the  pulse  is  therefore  diminished 
in  volume,  the  diminution  being  directly  proportionate  to  the 
degree  of  the  stenosis,  less  the  extent  of  the  compensatory 
changes  which  are  present.  In  addition  to  a  diminution  in 
volume,  the  pulse  wave  presents  other  modifications,  which 
will  be  presently  described.  I  must,  however,  here  point  out 
that  it  is  only  in  advanced  cases  of  aortic  stenosis  that  the 
supply  of  blood  to  the  arterial  system  is  so  much  diminished 
as  to  produce  important  alterations  in  nutrition  and  in  the 
functional  condition  of  the  peripheral  tissues  and  organs.  It 
must,  too,  be  remembered  that  the  subjects  of  aortic  stenosis 
are,  as  a  rule,  old  people,  who  lead  quiet,  inactive  lives,  and  in 
whom  all  the  tissue  changes  are  at  a  minimum. 

Symptoms — So  long  as  compensation  is  satisfactory,  and 


524  Diseases  of  the  Heart. 

the  stenosis  not  very  great,  there  are  few  if  any  symptoms. 
As  the  lesion  progresses,  and  the  supply  of  arterial  blood  to 
the  peripheral  organs  and  tissues  becomes  seriously  interfered 
with,  symptoms,  more  particularly  giddiness  or  fainting,  loss 
of  nerve  tone  and  of  muscular  power,  defective  (slow)  cere- 
bration, muscular  twitchings  or  even  epileptiform  convulsions 
— due  to  defective  supply  of  arterial  blood  to  the  brain — cold- 
ness of  the  hands  and  feet,  and  symptoms  indicative  of  general 
debility  and  impaired  nutrition,  may  occur.  When  compen- 
sation fails,  and  more  especial!}'  when  the  mitral  valve  gives 
way,  the  usual  symptoms  indicative  of  engorgement  of  the 
pulmonary  and  systemic  circulations  arise.  Cheyne-Stokes' 
respiration  sometimes  develops  and  ushers  in  a  fatal  termina- 
tion ;  in  other  cases  complications,  such  for  example  as 
apoplexy,  the  result  of  arterial  rupture,  may  arise  ;  indeed 
many  of  the  symptoms  in  typical  cases  of  aortic  stenosis  {i.e. 
pure  stenosis  in  old  people)  are  due  to  the  diseased  condition 
of  the  peripheral  vessels.  In  other  cases  accidental  symp- 
toms due  to  embolic  plugging  of  peripheral  vessels  occur. 

Physical  Signs. — The  primary  physical  sign  which  results 
from  aortic  stenosis  is  a  systolic  murmur  in  the  aortic  area, 
which  is  propagated  upwards  over  the  course  of  the  aorta 
and  into  the  great  vessels  of  the  neck.  (See  fig.  216.)  The 
murmur  is  usually  loud,  somewhat  harsh  in  character,  though 
sometimes  musical  ;  in  other  cases  it  is  soft  and  faint. 

The  second  sound  is  usually  faint  and  indistinct ;  in  those 
cases  in  which  the  valve  is  incompetent  as  well  as  contracted, 
it  is  of  course  replaced  by  a  diastolic  murmur. 

In  addition  to  the  systolic  murmur,  a  systolic  thrill  can 
often  be  felt  at  the  base  of  the  heart,  or  over  the  ascending 
thoracic  aorta. 

In  consequence  of  the  hypertrophy  of  the  left  vertricle, 
the  apex  beat  is  displaced  downwards  and  to  the  left  ;  the 
area  of  the  cardiac  dulncss  over  the  left  ventricle  is  increased,^ 


'   The  increased  cardiac  dulness  and  displacement  of  the  ape.\  are  not  so  great 
an  in  aortic  incompetence. 


Physical  Signs  of  Aortic  Stenosis. 


0^0 


and  a  powerful,  heaving,  but  slow  and  deliberate,  impulse  can 
in  many  cases  be  felt  on  palpating  the  praecordia.  The  apex 
beat  is  usually  weak  and  ill-defined,  sometimes  quite  imper- 
ceptible, a  fact  which  Traube  explains  by  supposing  that 
the  force  of  recoil  or  the  power  which  drives  the  heart  in 
the  direction  opposite  to  the  s\-stolic  outflow,  and  which  is 
one  of  the  factors  in  the  cardiac  impulse,  is  impeded  in  aortic 
stenosis  since  the  size  of  the  aortic  opening  is  smaller,  and 
the  resistance  to  the  outflow  greater  than  under  normal 
conditions.^ 


Flu.  216. — Outline  figure  showing  point  of  differential  maximum  intensity  (*) 
of  the  systolic  aortic  murmur  (aortic  stenosis)  ;  and  the  directions  in  which  it  is 
propagated. 

In  typical  cases,  the  pulse  is  slower  than  normal  ;  its 
volume  is  diminished,  but  unlike  the  small  pulse  of  mitral 
regurgitation  it  is  of  good  strength  (tension),  the  artery  being 
well  filled  during  the  ventricular  diastole  ;  the  pulse  of  aortic 
stenosis  is,  as  a  rule,  quite  regular  ;  its  sphygmographic 
characters  are  well  seen   in  the  following  tracings,  the  most 

'  Quoted  by  Rosenstein,  Ziewsseii's  Cyclopirdia.  vol.  vi.  p.  143. 


526  Disidscs  of  tJic  Heart. 

important  alterations  being  the  gradual  ascent  of  the  up- 
stroke corresponding  to  the  deliberate  contraction  of  the  left 
ventricle,  the  rounded  apex,  and  the  long  duration  of  both 
the  ventricular  systole  and  the  ventricular  diastole.  (See  figs. 
217  and  218.) 


Fig.   T.i'].—  Pressure  \\oz.  FiG.  218. — Pressure  \\  oz. 

Fig.   217.  —  Pulse  trading  in  aortie  s/euos/s. 

Fig.  218. — Pit/se  tracing  in  aortic  stenosis  and  dilatation  of  the  arch  of  the 
aorta,  the  latter  being  the  chief  lesion. 

l)u7£-;tosts.  —  \\'hen  a  sj'stolic  murniur  is  heard  at  the  base 
of  the  heart,  we  have  to  determine  : — 

1.  Is  the  murmur  generated  in  the  aorta  ? 

2.  If  it  is  generated  in  the  aorta,  is  it  due  to  organic  or 
functional  causes  ? 

3.  If  it   is  due   to  organic   causes,   does   it  depend   upon 
aortic  stenosis  ? 

4.  If  aortic   stenosis   is   present,  what   is  the  extent  and 
gravity  of  the  lesion  ? 

Step  A'o.  I. — Is  iJic  inunnttr generated  iji  the  acrta  ? 
There  is  seldom  any  difficulty  in  deciding  this  point, 
provided  that  an  accurate  survey  be  made  of  the  physical 
condition  of  the  heart  and  circulation.  Systolic  murmurs 
generated  at  the  mitral,  pulmonary,  and  tricuspid  orifices, 
may,  of  course,  be  heard  over  the  aortic  valve,  but  are  readily 
distinguished  by  attention  to  their  points  of  maximum  dif- 
ferential intensity,  their  direction  of  propagation,  their  sound 
characters,  and  the  secondary  results  which  they  produce  in 
the  heart  itself  and  in  the  peripheral  venous  and  arterial 
circulations.  The  chief  points  of  distinction  are  shown  in  the 
following  table  : — 


'^ 


Diagnosis  of  Aortic  Stenosis. 


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528  Diseases  of  iJie  Heart. 

Step  Xo.  2. — If  ilic  iiturnutr  is  generated  in  tlie  aorta,  is  it  eiiie 
to  organic  or  fnnetional  eanses  f 

111  conditions  of  anjcmia,  functional  murmurs  are  some- 
times generated  at  the  aortic  orifice,  and  it  is  very  important 
to  distinguish  cases  of  this  description  from  cases  in  which  the 
murmur  is  due  to  organic  changes  in  the  \alve  segments  or 
in  the  aortic  arch. 

Now,  it  is  quite  possible,  that  a  patient  who  is  affected 
with  aortic  stenosis  may  at  the  same  time  be  anaemic  ;  and  in 
cases  of  this  description  it  may  be  difficult  or  impossible  to 
arrive  at  a  positive  conclusion  as  to  the  cause  of  a  systolic 
murmur  heard  in  the  aortic  area.  There  is  usually  no 
difficulty  in  distinguishing  uncomplicated  cases  (pure  ca.ses  of 
aortic  stenosis  on  the  one  hand  from  pure  cases  of  anaemic 
basic  murmurs,  such  as  arc  met  with  in  the  course  of  chlorosis, 
or  progressive  pernicious  anaemia,  on  the  other)  by  attention 
to  the  following  points  : — 

1.  Tlie  age  and  general  condition  of  tlie  patient. —  In 
chlorosis  and  progressive  pernicious  anaemia,  which  arc  the 
forms  of  general  anjemia  in  which  basic  murmurs  are  most 
apt  to  arise,  the  patient  is,  as  a  rule,  young,  or  in  active 
adult  life,  the  skin  often  has  a  lemon  yellow  tinge,  and 
there  is  no  wasting  of  subcutaneous  fat.  Whereas  in  the 
anaemia  which  is  associated  v.'ith  aortic  stenosis,  the  patient  is 
generally  old,  as  a  rule  spare,  the  subcutaneous  fat  in  par- 
ticular being  generally  scanty,  and  general  atheroma  often 
present. 

2.  77ic  condition  of  tlic  left  voitricle,  and  of  the  right  heart. 
■ — In  anaemia  the  left  ventricle  is  dilated  rather  than  hyper- 
trophied,  whereas  in  aortic  stenosis  the  hypertrophy  is 
generally  pure.  In  ansmia  the  right  heart  is  also  dilated 
and  hypertrophied,  whereas  in  aortic  stenosis  it  is  u.sually 
quite  normal. 

3.  The  character  of  tlie  pnlse. — In  aortic  stenosis  the  left 
ventricle  contracts  with  much  deliberation,  the  pulse  is  slower 
than  normal,  and  the  apex  of  the  sphygmographic  tracing  is 
usually  rounded  ;  whereas  in  anaemia  the  ventricle  contracts 
in  a  .sharp,  irritable   manner,  especiall)'  when    the   patient   is 


Diagnosis  of  A  or  lie  Stenosis.  529 

agitated  ;  the  frequency  of  the  cardiac  contraction  is,  under 
such  circumstances,  considerably  increased,  and  the  apex  of 
the  sphygmographic  tracing  is  more  pointed  than  normal. 
Contrast  figure  217  with  figures  219  and  220. 


Fig.  219.  Fig.  220. 

Figs.    219  and  22.0.—  Pulse  traciii;^;^  from  a  case  of  progressive  pernicious  aiunuia. 

Fig.  220  was  taken  shortly  before  death  ;  the  artery  is  very  empty  during 
diastole. 

4.  Tite  sound  ciiaracter  of  the  iininnnr,  tlie  preseiiee  of  a 
systolic  basic  thrill,  and  other  uiiirniurs  over  the  heart. — The 
aortic  murmur  of  ansemia  is  almost  invariably  soft  and  badly 
propagated,  and  is  often  quite  inaudible  in  the  carotids, 
whereas  the  murmur  of  organic  stenosis  is  usually  loud  and 
harsh,  and  is  well  propagated  over  the  course  of  the  aorta 
and  into  the  great  vessels  of  the  neck. 

A  systolic  thrill  can  frequently  be  felt  in  aortic  stenosis. 
An  aortic  murmur  due  to  anaemia  is  usually  (  ?  invariably) 
accompanied  by  a  venous  hum  in  the  neck,  by  a  pulmonary 
systolic  murmur,  and  very  often  by  mitral  and  tricuspid  systolic 
murmurs.  An  aortic  systolic  murmur  due  to  stenosis  is  often 
associated  with  a  diastolic  aortic  murmur. 

5.  The  effects  of  treatment. — Many  cases  of  anaemia  are, 
as  we  have  previously  seen,  completely  curable  ;  in  cases  of 
this  description  the  basic  murmur  completely  disappears 
under  treatment,  whereas  in  aortic  stenosis  the  lesion  alwa>'s 
remains. 

6.  The  nature  of  the  symptoms.  —  In  anaemic  cases  the 
least  exertion  produces  shortness  of  breath  and  palpitation, 
and  there  is  often  some  swelling  of  the  feet.  These  symptoms 
are  not  present  in  aortic  stenosis,  although  they  may,  as  wc 
have  seen,  occur  in  the  later  stages  of  the  case. 

L  L 


530  Dheases  of  tJic  Heart. 

Step  No.  3. —  The  murmur  is  due  to  organic  causes  ;  does  it 
depend  upon  aortic  stenosis  f 
The   other    organic    conditions   which    may    produce    an 
aortic  systolic  murmur,  independently  of  disease  of  the  aortic 
orifice,  are  : — 

1.  Dilatation  of  tlic  ascending  thoracic  aorta. — Dilatation 
of  the  aorta  (which  is  frequently  associated  with  aortic 
stenosis)  usually  gives  rise  to  increased  dulness  over  the 
course  of  the  aorta,  increased  pulsation  in  the  aortic  notch  ; 
a  systolic  thrill,  in  addition  to  the  murmur,  is  usually  present, 
and  there  may  be  symptoms  and  signs  indicative  of  the  pres- 
sure of  the  dilated  vessel  upon  the  surrounding  structures  and 
parts.  When  the  aortic  segments  are  healthy,  the  aortic  second 
sound  is  loudly  accentuated,  whereas  in  aortic  stenosis  it  is 
usually  weakened  or  effaced.  Both  conditions  may  be  accom- 
panied by  a  diastolic  aortic  murmur,  indicative  in  the  former, 
of  relative  incompetence,  in  the  latter,  of  regurgitation  due  to 
organic  changes  in  the  valve  flaps.^ 

2.  Constriction  oftlie  aorta  by  the  pressure  of  an  intra-tJioracic 
growth. — Cases  of  this  description  could  hardly  be  mistaken 
for  cases  of  pure  stenosis  {i.e.  stenosis  without  aortic  dilata- 
tion) ;  there  may  be  considerable  difficulty  in  distinguish- 
ing them  from  aneurismal  dilatation  of  the  aortic  arch,  but 
this  point  will  be  afterwards  considered  in  detail  (see  page  726). 

Prognosis. — Aortic  stenosis  is  the  least  serious  of  all 
the  organic  valvular  lesions  of  the  heart,  and  its  average 
duration  is  longer  than  that  of  other  lesions  ;  it  is  often 
unattended  by  any  serious  or  distressing  symptoms,  and  it 
has  not  the  same  tendency  to  produce  sudden  death  as  aortic 
regurgitation. 

The  gravity  of  each  individual  case  must  of  course  be 
determined  by  observing  : — 

(i)  The  extent  of  the  lesion.  (The  amount  of  the  second- 
ary hypertrophy  of  the   left  ventricle,  and  the  characters  of 

'  The  exact  nature  of  the  symptoms  and  physical  signs  which  characterise 
dilatation  of  the  aorta  will  be  more  particularly  described  when  the  diseases  of  the 
aorta  are  treated.     (See  p.  726.) 


Treatvicnt  of  Acviic  Stenosis.  531 

the  pulse,  are  the  points  to  which  attention  must  be  specially 
directed  in  order  to  determine  the  extent  of  the  lesion.) 

(2)  The  capabilities  of  compensation  and  resistance. 

(3)  The  presence  of  complications.  All  of  these  points 
have  been  so  fully  considered  in  treating  of  the  other  valvular 
lesions,  that  they  need  not  be  again  detailed. 

Treatvient. — The  general  plan  of  treatment  which  has 
been  recommended  for  aortic  regurgitation  must  be  carried 
out.  When  the  left  ventricle  begins  to  fail,  digitalis  must  be 
freely  given  ;  but  it  must  be  discontinued  as  soon  as  its  tonic 
effect  has  been  produced,  the  prolonged  administration  of  the 
drug  increases  the  arterial  tension,  and  theoretically,  at  all 
events,  may  be  supposed  to  increase  the  risk  of  rupture  of  the 
diseased  peripheral  vessels. 

TRICUSPID   INCOMPETENCE. 

Definition.  —  Tricuspid  incompetence  includes  all  those 
conditions  which  interfere  with  the  perfect  closure  of  the 
tricuspid  valve  apparatus,  and  allow  a  regurgitant  blood 
current  to  pass  from  the  cavity  of  the  right  ventricle  into  that 
of  the  right  auricle  during  the  ventricular  systole. 

ALtiology  and  Pathology. — The  tricuspid  valve  apparatus 
is  constructed  on  the  same  plan  as  the  mitral  valve  apparatus,^ 
the  only  differences  being  (i)  that  the  tricuspid  valve  has  three 
segments,  and  (2)  that  the  muscular  wall  of  the  right  ventricle, 
or,  as  we  may  term  it,  the  tricuspid  sphincter,  is  thinner  and 
weaker  than  the  muscular  wall  of  the  left  ventricle  (or  mitral 
sphincter),  and  that  relative  and  muscular  incompetence  arc, 
therefore,  more  readily  produced  at  the  tricuspid  than  at  the 
mitral  orifice  ;  it  is  indeed  probable,  that  tricuspid  incom- 
petence frequently  occurs  even  in  perfect  health  as  the  result 
of  the  temporary  over-distention  of  the  right  ventricle.  King 
was  the  first  to  direct  attention  to  this, — the  safety  valve  action 
of  the  tricuspid,  as  he  termed  it. 

'    The   reader   is  recommended    to   refer   to   the   detailed    description    of   the 
anatomy  and  physiology  of  the  mitral  valve  apparatus  described  on  p.  421. 


532  Diseases  of  the  Heart. 

Tricuspid  incompetence  may,  therefore,  result  from  : — 

(i)  Organic  changes  in  the  valve  segments. 

(2)  '  Muscular'  and  '  relative'  incompetence. 

Now  incompetence  due  to  organic  changes  in  the  tricuspid 
valve  segments  is  rare  ;  it  occasionally  occurs  as  a  congenital 
condition,  i.e.  as  the  result  of  inflammatory  changes  during 
intra-uterine  life  ;  sometimes  also  as  the  result  of  endocarditis 
in  after  life  ;  and  the  same  causes  which  produce  endocarditis 
at  the  mitral  orifice^  are  the  causes  of  tricuspid  endocarditis. 
The  pathological  appearances  in  both  conditions  (tricuspid 
and  mitral  endocarditis)  are  the  same,  I  must  further  repeat 
that  I  am  disposed  to  think  that  acute  inflammation  of  the 
tricuspid  valve  is  much  more  common  than  is  generally 
supposed  ;  and  that,  like  the  endocarditis  of  chorea,  it  usually 
subsides  without  leaving  any  permanent  structural  changes. 

'  Muscular '  and  '  relative  '  incompetence  of  the  tricuspid 
are,  on  the  contrary,  more  common  than  'muscular'  and 
'  relative '  incompetence  of  the  mitral,  and  may  result  from  : — - 

(a)  Structural  changes  in  the  muscular  wall  of  the  right 
heart,  amongst  which  fatty  changes,  the  result  of  anaemia, 
are  perhaps  the  most  important.  In  these  cases  we  may 
term  the  condition  primary  'muscular'  and  'relative'  incom- 
petence. 

(b)  Dilatation  of  the  cavity  of  the  right  ventricle,  the 
result  of  an  obstruction  in  front,  i.e.  in  the  lungs  or  at  the 
mitral  orifice.  In  these  cases,  in  which  we  may  term  the 
condition  secondary  '  muscular '  and  '  relative  '  incompetence, 
there  are  usually  also  degenerative  changes  in  the  cardiac 
muscle,  in  consequence  of  which  the  right  ventricle  becomes 
dilated  rather  than  hypertrophied.  I  must  repeat,  that  this 
form  of  tricuspid  regurgitation,  which  depends  upon  dilatation 
and  degeneration  of  the  right  ventricle,  and  which  is  second- 
ary to  an  obstruction  either  in  the  lungs  or  at  the  mitral 
orifice,  is  extremely  common  ;  and  since  the  primary  causes  of 
the  condition  (i.e.  pulmonary  or  mitral  lesions)  are  in  some 
cases  completely  curable,  the  tricuspid  incompetence  may  also 
be  a  temporary-  and  curable  condition. 

'   Sec  p.  425. 


Pathology  of  Tric2ispid  Incompetence.  533 

Pathological  physiology.  —  The  first  effect  of  tricuspid 
regurgitation  is  to  allow  a  regurgitant  blood  current  to  pass 
from  the  cavity  of  the  right  ventricle  to  that  of  the  right 
auricle  during  the  ventricular  systole.  The  second  is  to 
produce  a  series  of  changes  in  the  heart  and  circulation,  which 
are  as  follows  : — 

Effect  on  the  heart. — The  right  auricle  becomes  dilated, 
and  in  some  cases  also  hypcrtrophied.  The  hypertrophy  is, 
however,  as  a  rule,  slight,  in  consequence  of  the  facts,  firstly, 
that  the  wall  of  the  auricle  is  extremely  thin  and  incapable 
of  great  hypertrophy  ;  and  secondly,  and  more  particularly, 
that  in  cases  of  tricuspid  incompetence  the  conditions  for  the 
production  of  satisfactory  hypertrophy  (a  healthy  condition  of 
the  system  as  a  whole  and  of  the  heart  in  particular)  are 
seldom  present.  In  many  cases  the  muscle  fibre  is  degen- 
erated, and  the  nutrition  of  the  heart  and  the  general  powers 
of  compensation  and  resistance  are  weakened  by  the  primary 
disease  (such  for  example,  as  long  continued  venous  conges- 
tion, the  result  of  a  chronic  mitral  lesion),  on  the  top  of 
which,  so  to  speak,  the  tricuspid  regurgitation  is  added. 

Theoretically,  the  right  ventricle  ought  to  become  hypcr- 
trophied and  dilated  as  the  result  of  tricuspid  incompetence, 
just  as  the  cavity  of  the  left  ventricle  becomes  dilated  and 
hypcrtrophied  as  the  result  of  mitral  incompetence ;  as  a 
matter  of  fact,  however,  h}43ertroph}^  does  not  as  a  rule 
occur,  firstly,  because  the  powers  of  compensation  are  feeble  ; 
secondly,  because,  in  secondary  cases  at  all  events,  the  right 
ventricle  has  already  put  forth  all  its  efforts,  and  has  become 
as  fully  hypcrtrophied  as  it  can  become  (in  order  to  overcome 
the  obstruction  in  front)  before  the  tricuspid  incompetence  is 
established. 

Effect  on  the  circulation  in  front. — As  soon  as  tricuspid 
incompetence  is  established,  the  quantity  of  blood  propelled 
into  the  pulmonary  circuit  becomes  diminished  ;  the  left  heart 
consequently  receives  less  blood,  and  the  supply  of  blood  to 
the  systemic  arterial  circulation  is  lessened. 

Efi'ect  on  the  venous  eireulation. — The  effect  which  tricuspid 
incompetence  produces  upon  the  systemic  venous  circulation 


534  Diseases  of  the  Heart. 

is  extremely  serious.  At  each  contraction  of  the  right  ventricle 
a  back-wash  (the  amount  of  the  regurgitant  current  being 
directly  proportionate  to  the  extent  of  the  tricuspid  leak  and 
the  power  of  the  right  ventricle)  passes  through  the  cavity  of  the 
right  auricle  into  the  superior  and  inferior  venae  cavae  ;  in  fact, 
with  the  occurrence  of  tricuspid  regurgitation  the  last  cardiac 
barrier,  which  protects  the  systemic  venous  circulation  from  the 
injurious  effects  of  backward  pressure,  is  removed,  and  all  the 
secondary  changes  in  the  peripheral  tissues  and  organs,  which 
I  have  detailed  under  the  head  of  mitral  incompetence,  be- 
come seriously  aggravated.  The  engorgement  of  the  veins  is 
now,  it  must  be  remembered,  no  longer  passive,  but  at  each 
systole  of  the  heart  a  regurgitant  current  is  forced  right  into 
the  venous  trunks,  and  the  peripheral  tissues  and  organs  are 
then  only  protected  from  the  direct  effects  of  the  '  back-wash  ' 
by  the  valves  of  the  veins  themselves. 

Clinical  History. — Tricuspid  incompetence  is  (as  I  have  so 
repeatedly  stated),  with  rare  exceptions,  a  secondary  condition. 
The  symptoms  therefore  which  it  produces  are,  in  the  great 
majority  of  cases,  superadded  to  the  symptoms  of  the  primary 
affection  to  which  the  tricuspid  incompetence  is  secondary. 
The  exact  nature  of  the  primary  symptoms  varies,  of  course, 
with  the  exact  nature  of  the  primary  lesion,  but,  for  our 
present  purpose,  we  may  suppose  that  the  primary  condition 
is  a  progressive  organic  lesion  of  the  mitral  orifice  (mitral 
stenosis  or  mitral  incompetence).  With  the  occurrence,  then, 
of  tricuspid  incompetence,  the  dropsy  and  effusion  into  the 
serous  cavities  become  greater,  the  dyspnoea  and  other 
respiratory  troubles  are  increased,  and  haemoptysis  due  to 
pulmonary  apoplexy  is  apt  to  arise  ;  the  symptoms  due  to 
venous  engorgement  of  the  digestive  and  urinary  organs  and 
of  the  nerve  centres  become  aggravated  ;  in  short  all  the 
more  serious  symptoms,  which  I  have  previously  detailed  as 
characteristic  of  the  terminal  periods  of  a  progressive  mitral 
lesion,  are  fully  developed.  In  cases  of  this  description  (pro- 
gressive mitral  disease  to  which  tricuspid  regurgitation  is  super- 
added) a  fatal  termination  is  soon  reached. 


Physical  signs  of  Tricuspid  lucoinpctencc.       535 

When  the  tricuspid  incompetence  depends  upon  temporary 
and  curable  conditions,  the  severity  of  the  symptoms  is  not  so 
great ;  in  conditions  of  ansemia,  for  example,  a  slight  degree 
of  incompetence  at  the  tricuspid  orifice  is  of  frequent  occur- 
rence, and  is  not  necessarily  attended  with  serious  symptoms. 
It  must,  too,  be  remembered,  that  temporary  tricuspid  re- 
gurgitation may  occur  in  the  course  of  organic  lesions  of  the 
mitral  orifice,  as  the  result,  for  example,  of  an  attack  of 
acute  bronchitis  or  any  other  complication  which  produces  a 
temporary  failure  of  compensation  and  throws  a  sudden  strain 
on  the  right  heart.  In  estimating  the  prognosis  of  tricuspid 
incompetence,  each  individual  case  must  be  judged  on  its  own 
merits,  and  the  exact  causation  of  the  tricuspid  lesion  taken 
into  account. 

Physical  signs. — The  primary  physical  signs  indicative  of 
tricuspid  regurgitation  are: — (i)  a  systolic  murmur  in  the  tri- 
cuspid area,  and  (2)  true  venous  pulsation  in  the  neck. 

The  murmur  is  soft  and  blowing  ;  its  point  of  maximum 
differential  intensity  is  the  lower  end  of  the  sternum  or 
adjacent  costal  cartilages  ;  and  its  direction  of  propagation 
upwards  and  to  the  right.     (See  fig.  221.) 

The  venoKS  pulsation  is  usually  best  marked  in  the  external 
jugular  vein  on  the  right  side,  but  is  frequently  also  seen  in 
the  corresponding  vein  on  the  left  side  and  in  the  internal 
jugulars.  The  pulsation  is  synchronous  with  the  contraction 
of  the  right  ventricle,  and  usually,  but  not  invariably,  persists 
after  the  lower  part  of  the  vein  has  been  emptied  by  the 
pressure  of  the  finger,  the  return  current  of  blood  being 
arrested  by  pressure  on  the  vein  in  the  manner  previously 
described.  Dr  Hilton  Fagge  points  out,  that  in  those  cases 
in  which  the  right  ventricle  is  acting  feebly  or  in  which  the 
tricuspid  leak  is  slight,  the  back  wave  in  the  veins  may  not  be 
sufficiently  strong  to  distend  the  whole  of  the  emptied  vein, 
and  so  pulsation  in  the  neck  may  not  be  observed.  Again, 
in  the  slighter  degrees  of  tricuspid  incompetence,  the  valves 
at  the  junction  of  the  external  jugular  and  subclavian  veins 
may  still    be   competent  ;    and   in   cases  of  this  description 


536  /J/scasrs  of  the  Heart. 

simple   distention   or    pulsation    in   the  venous    bulb,   is   only 
observed. 


Fig.   221. — Outline  figure  showing  point  of  difterential  maximum  intensity  {*)  of 
the  systolic  tricuspid  murmur. 

In  addition  to  the  venous  pulsation  in  the  neck,  true 
venous  pulsation  in  the  liver,  causing  an  expansile  pulsation 
of  the  organ  synchronous  with  the  contractions  of  the  right 
ventricle,  is  in  many  cases  also  present. 

l^esides  the  systolic  tricuspid  murmur  and  venous  pulsa- 
tion, increased  dulness  over  the  lower  end  of  the  sternum  and 
adjacent  costal  cartilages  (due  to  enlargement  of  the  right 
heart)  is  also  observed  ■}  and  the  impulse  of  the  right  heart 
can  often  be  seen  and  felt  in  the  pit  of  the  epigastrium.  The 
radial  pulse  is  small,  weak,  and  very  often  irregular,  in  fact, 
it  usually  presents  the  characters  which  are  present  in 
advanced  stages  of  mitral  regurgitation. 

'   When  the  lungs  are  empliysematous,  increased  dulness  over  the  prxcordia 
may  not  be  present. 


IJiao/iosis  of  l^riciispui  Incompetence.  537 

Diagnosis.  —  The  steps  in  the  diagnosis  of  tricuspid 
regurgitation  are  : — 

(i)  Is  tricuspid  incompetence  actually  present? 

(2)  If  tricuspid  incompetence  is  present,  is  the  condition 
primary  {i.e.  due  to  changes  originating  in  the  right  heart)  or 
secondary  ? 

(3)  If  secondary,  what  is  the  nature  of  the  primary- 
condition  ? 

(4)  What  is  the  extent  and  gravity  of  the  lesion  ? 

Step  No.  I . — Is  tricuspid  ijicoiupctence  actually  present  ? — 
When  a  systolic  tricuspid  murmur  and  true  venous  pulsation 
in  the  neck  or  in  the  liver  are  present,  this  question  is  at  once 
decided  in  the  affirmative,  provided,  of  course,  that  the 
observer  is  satisfied  that  the  systolic  murmur  is  actually  a 
tricuspid  murmur  ;^  and  that  the  venous  pulsation  is  not  one 
of  the  false  forms  of  venous  pulsation  which  have  been  pre- 
viously described. - 

Step  No.  2. — If  tricuspid  regurgitation  is  present,  is  the 
condition  primary  (i.e.  due  to  cliangcs  originating  in  tJie  right 
heart)  or  secondary  to  some  other  condition  ? 

Step  N^o.  3. — If  secondary,  zvJiat  is  the  exact  nature  of  the 
primary  lesion  ? 

In  attempting  to  solve  these  questions  it  must  be  remem- 
bered : — (i)  that  primary  tricuspid  regurgitation  {i.e.  tricuspid 
incompetence  due  to  changes  originating  in  the  right  heart) 
is  comparatively  rare  ;.  whereas  the  secondary  form  of  the 
lesion  is  common  ;  and  (2)  that  the  primary  form  of  the  disease 
is  occasionally  (more  frequently  I  believe  than  is  generally 
allowed)  met  with  as  an  acute  affection  in  the  course  of 
rheumatic  fever  and  as  a  chronic  lesion  in  anaemia  and  other 
conditions  in   which  the  muscular  fibre  of  the  right  heart  is 


'  The  differential  diagnosis  of  pericartlial  murmurs  and  endocardial  {e.g. 
tricuspid)  murmurs  is  set  forth  on  page  331  ;  while  the  points  of  distinction 
between  the  different  forms  of  systolic  endocardial  murmurs  are  detailed  on 
page  527. 

^  See  page  2gi. 


538  Diseases  of  the  Heart. 

degenerated.  It  is  also  sometimes  associated  with  congenital 
stenosis  of  the  pulmonary  artery.^ 

The  circumstances  under  which  the  tricuspid  regurgita- 
tion is  established,  the  condition  of  the  pulmonary  second 
sound,  and  more  especially  the  presence  or  absence  of  any 
disease  in  the  lungs  or  at  the  mitral  orifice,  likely  to  produce 
secondary  changes  in  the  right  heart,  are  the  points  to  which 
attention  must  be  directed  in  order  to  determine  whether  the 
tricuspid  lesion  is  primary  or  secondary. 

In  some  cases  in  which  cyanosis,  dropsy,  and  tricuspid 
regurgitation  arc  present,  it  may  be  difficult  to  determine 
whether  the  primary  lesion  is  a  congenital  cardiac  affection, 
such  as  stenosis  of  the  pulmonary  artery  with  a  patent  con- 
dition of  the  foramen  ovale  ;  or  a  primary  affection  of  the  lungs, 
such  as  chronic  bronchitis  and  emphysema  ;  or  an  advanced 
mitral  stenosis.  The  points  to  which  attention  is  to  be  directed 
in  order  to  solve  this  question  are  given  on  page  555. 

Step  No.  4. —  What  is  the  extent  and  gravity  of  the  lesion  ? 
— This  question  Avill  be  more  appropriately  considered  under 
the  prognosis,  to  which  I  now  pass. 

Prognosis.  — In  considering  the  prognosis  of  tricuspid  in- 
competence it  is  essential  to  remember  (i)  that  in  some  cases 
the  regurgitation  is  due  to  temporary  and  curable  conditions, 
such  for  example  as  a  chlorotic  condition  of  the  right  heart  ; 
and  (2)  in  other  cases  it  is  secondary  to  progressive  and 
incurable  organic  disease,  such  for  example  as  mitral  stenosis. 

In  order  to  give  a  satisfactory  opinion,  therefore,  as  to  the 
significance  of  tricuspid  regurgitation  in  any  individual  case, 
it  is  essential,  in  the  first  place,  to  determine  the  exact  cause 
of  the  condition,  and  whether  that  cause  is  removable  {i.e. 
curable)  or  not.  In  deciding  this  question  attention  must 
be  directed  to  the  points  detailed  in  speaking  of  the  diagnosis 

'  In  many  of  these  cases  the  dilatation  of  the  right  heart,  on  which  the  tricuspid 
incompetence  partly  depends,  is  due  to  a  double  cause,  viz.,  degeneration  of  the 
wall  of  the  right  ventricle  and  obstruction  in  front  (in  the  lungs  or  at  the  mitral 
orifice) ;  in  short,  in  many  cases  of  this  description,  the  tricuspid  incompetence  is 
partly  primarj'  and  partly  secondary. 


Triciispid  Stenosis.  539 

of  tricuspid  incompetence  and  the  diagnosis  and  prognosis  of 
'  relative '  and  '  muscular '  incompetence  of  the  mitral  orifice. 

If  we  come  to  the  conclusion  that  the  tricuspid  regurgita- 
tion is  due  to  incurable  conditions  (if,  for  example,  it  occurs 
in  the  course  of  advanced  progressive  mitral  disease),  the 
prognosis  is  most  unfavourable  ;  indeed  tricuspid  incompetence 
is,  under  such  circumstances,  of  the  gravest  possible  signi- 
ficance, for,  with  the  removal  of  the  tricuspid  barrier,  the 
full  force,  so  to  speak,  of  the  backward  pressure  falls  directly 
upon  the  venous  system,  and  all  the  grave  symptoms  which 
result  from  venous  engorgement  become  seriously  aggravated. 

Treatment. — Tricuspid  incompetence  is  to  be  treated  in 
the  same  way  as  mitral  incompetence.     (See  page  469.) 

TRICUSPID   STENOSIS. 
Definition. — Narrowing  of  the  tricuspid  orifice. 

Aetiology  and  PatJiotogy. — Stenosis  of  the  tricuspid  orifice 
is  sometimes,  though  very  rarely,  present  at  the  time  of  birth. 
In  cases  of  tricuspid  stenosis,  in  which  the  condition  results 
from  foetal  endocarditis,  the  mitral  valve  is  generally  also 
constricted  ;  in  other  cases,  pulmonary  stenosis  and  a  patent 
condition  of  the  foramen  ovale  are  present. 

In  the  majority  of  cases  of  tricuspid  stenosis,  the  condi- 
tion probably  results  from  endocarditis  after  birth.  Slight 
degrees  of  narrowing  are  probably  by  no  means  so  rare  as 
was  at  one  time  supposed.  Dr  Bedford  Fenwick,  for  example, 
has  stated  that  forty-six  cases  of  tricuspid  stenosis  have  been 
recorded  since  the  year  1825,  and  from  an  analysis  of  these 
cases  he  concludes  that  the  greater  number  of  them,  at  all 
events,  were  due  to  changes  after  birth  ;  in  all  of  the  forty- 
six  cases,  the  mitral  valve  was  similarly  affected,  and  in  nearly 
all,  the  degree  of  constriction  was  greater  at  the  mitral  than 
at  the  tricuspid  orifice.^ 

Professor  Gairdner  has  recorded  a  case  (the  first  case  I 
ibelieve  in  which  the  diagnosis  of  tricuspid  stenosis  was  made 

'   Lancet,  January  22,  18S1,  p.  137. 


540  D/si'ascs  of  iJic  Heart. 

during  life)  in  which  the  narrowing  was  due  to  the  pressure  of 
a  tumour  on  the  valve  segments. 

The  acquired  (non-congenital)  form  of  tricuspid  stenosis 
is  like  mitral  stenosis,  much  more  common  in  females  than 
in  males.  The  causes  of  the  two  conditions  (/>.  of  mitral 
stenosis  and  tricuspid  stenosis)  and  the  structural  changes  in 
the  valve  segments,  are  the  same  ;  the  extreme  narrowing, 
however,  which  is  so  common  at  the  mitral,  is  extremely  rare 
at  the  tricuspid  orifice,  a  fact  which  is  probably  to  be  ex- 
jilained  by  the  lesser  amount  of  strain  to  which  the  segments 
of  the  tricuspid  valve  are  subjected. 

PatJiological pliysiology. — The  effect  of  tricuspid  stenosis  is, 
of  course,  to  interfere  with  the  passage  of  the  blood  from  the 
right  auricle  to  the  right  ventricle,  and  so  through  the  lungs 
to  the  left  heart.  When  the  stenosis  is  congenital,  and 
associated  as  it  sometimes  is  with  pulmonary  stenosis,  the 
foramen  ovale  remains  open,  and  the  blood  makes  a  short  cut 
through  this  channel  to  the  left  heart. 

When  the  condition  is  due  to  changes  after  birth,  the  left 
auricle  is  almost  always  very  much  dilated.  The  free  supply 
of  blood  to  the  lungs  is  interfered  with  in  proportion  to  the 
degree  of  the  stenosis,  and  engorgement  of  the  systemic 
venous  circulation  is,  of  course,  present.  Probably  in  all 
cases  (in  all  cases,  at  all  events,  of  the  acquired  form),  the 
tricuspid  valve  is  also  incompetent. 

Symptovis. — In  the  congenital  cases,  the  symptoms  are 
practically  identical  with  those  of  pulmonary  stenosis,  which 
I  will  presently  describe.  In  the  acquired  form,  the  symptoms 
arc  usually  those  of  mitral  disease  plus  those  of  tricuspid 
incompetence. 

Physical  Signs. — In  one  or  two  cases  which  have  been 
reported,  a  presystolic  murmur  in  the  tricuspid  area  has  been 
])rcsent,  and  the  condition  has  been  diagnosed  during  life  ; 
in  the  great  majority  of  cases  the  condition  has  not  been 
recognised   during   life,   or  has   been   diagnosed   as    tricuspid 


Diagnosis  of    Tricuspid  Slciiosis.  541 

regurgitation — the  stenosis  is  seldom  sufficiently  great  to  cause 
a  presystolic  murmur,  but  a  systolic  murmur  due  to  associated 
incompetence  is  very  frequently  present. 

Diagnosis. — The  condition  can  only  be  recognised  with 
certainty  when  a  presystolic  murmur  distinctly  localised  to 
the  tricuspid  area  is  present.  The  condition  may  be  suspected 
when  signs  of  great  dilatation  of  the  right  auricle  and  engorge- 
ment of  the  systemic  venous  circulation  are  present ;  and 
when  the  tricuspid  incompetence,  which  is  almost  invaribly 
present  in  cases  of  tricuspid  stenosis,  does  not  seem,  sufficient 
to  account  for  these  conditions  (in  a  case  of  tricuspid  incom- 
petence, for  instance,  in  which  the  right  auricle  and  venous 
circulations  are  much  engorged,  but  in  which  the  venous  pulse 
in  the  neck  is  feebly  marked).  If,  again,  there  is  reason 
to  believe  that  the  tricuspid  incompetence  is  due  to  organic 
changes  in  the  valve  segments,  rather  than  to  relative  or  mus- 
cular incompetence,  the  presence  of  some  degree  of  stenosis 
as  well  as  incompetence  may  be  legitimately  suspected. 

Prognosis. — The  prognosis  is  unfavourable  ;  the  majority 
of  cases  terminate  fatally  soon  after  the  symptoms  of  sys- 
temic venous  engorgement  have  become  prominent. 

Treatment. — Little  can  be  done  in  the  way  of  treatment  ; 
the  same  means  which  have  been  recommended  for  the  treat- 
ment of  advanced  mitral  disease,  and  of  tricuspid  incom- 
petence, are  to  be  adopted. 

PULMONARY   STENOSIS. 

Aitiology. — Stenosis  of  the  pulmonary  artery  is  occasionall}', 
though  very  rarely,  produced  after  birth,  but  is  more  frequent 
as  the  result  of  disease  or  arrested  development  during  intra- 
uterine life.  Indeed  stenosis  or  complete  occlusion  (atresia)  of 
the  pulmonary  orifice  or  pulmonary  artery,  with  certain  second- 
ary changes,  such  as  a  patent  foramen  ovale,  or  an  imperfect 
intra-ventricular  septum,  is  the  condition  which  is  present  in 
the  great  majority  of  cases  of  congenital  heart  disease. 


54-  Diseases  of  tJie  Heart. 

Acquired {x\or\-zovL^Q:\\\X.2X)  stenosis  is  occasionally  produced 
in  the  course  of  acute  ulcerative  endocarditis,  the  orifice  being 
obstructed  by  luxuriant  vegetations  ;  it  is  sometimes  also 
caused  by  chronic  inflammator)-  and  atheromatous  changes  at 
the  pulmonary  orifice,  identical  in  character  and  results  with 
the  chronic  inflammatory^  and  atheromatous  changes  which 
are  so  veiy  much  more  frequent  at  the  orifice  of  the  aorta. 
I  must  repeat,  however,  that  pulmonar}'  stenosis  due  to  any 
of  these  conditions  is  extremely  rare. 

Congenital  stenosis  usually  results  from  fcetal  endocarditis 
or  myocarditis  ;  but  it  ma}-  probably  also  be  due,  as  Peacock 
theorised,  to  defective  development  of  the  bronchial  arch  from 
which  the  ductus  arteriosus  is  formed  ;  in  such  a  condition  the 
pulmonary  arter}'  would  of  course  receive  a  much  smaller 
supply  of  blood  than  usual,  and  would  therefore  be  imper- 
fectly developed.^ 

Pathology. — In  some  cases  it  is  extremely  difficult  to  say 
from  the  mere  pathological  characters  of  the  lesion,  whether 
the  stenosis  belongs  to  the  congenital  or  to  the  acquired 
forms  of  the  disease.  When  the  lesion  is  limited  to  the  valve 
segments  and  basal  ring,  the  condition  is  probably  acquired, 
for  foetal  endocarditis  is  rarely  so  limited,  and  the  congenital 
form  of  the  disease  is  generally,  if  not  always,  attended  by 
other  changes,  such  as  alterations  in  the  trunk  of  the  pul- 
monary artery,  the  sinus  arteriosus  of  the  ventricle,  and  the 
persistence  of  some  of  the  foetal  openings  in  the  heart.  Kuss- 
maul,  quoted  by  Lebert,  sums  up  the  points  of  distinction 
between  the  two  forms  in  the  following  propositions  :  '  This 

'  During  intra-uterine  life,  the  right  heart  is,  as  I  have  pre\-iously  explained, 
much  more  apt  to  be  afiected  by  inflammation  (endocarditis  and  myocarditis)  than 
the  left ;  the  greater  liability  being  due  to  the  fact  that  before  birth  the  valves  on 
the  right  side  are  subjected  to  more  strain  than  those  on  the  left,  the  right  heart 
being  more  active  than  the  left.  Peacock  further  supposes  that  in  consequence  of 
the  temporary  alterations  of  the  blood  pressure  which  are  apt  to  occur  in  the 
umbilical  arteries  and  placenta,  disease  at  the  base  of  the  pulmonary  artery  (which 
is  directly  continuous  with  the  descending  aorta  and  umbilical  arteries)  may  be 
established,  just  as  disease  of  the  base  of  the  aorta  and  aortic  valves  may  result 
in  after  life  from  increased  blood  pressure  (sudden  strain,  etc. ),  within  the  systemic 
arterial  system. 


PatJiology  of  Pulmonary  Stenosis.  543 

affection  of  the  heart  is  the  more  surely  congenital : — ist,  when 
the  birth  was  near  the  normal  end  of  pregnancy  ;  2d,  the 
sooner  after  birth  cyanosis  and  other  tokens  of  heart  disease, 
collectively  called  physical  symptoms  of  stenosis  of  the 
pulmonary  artery,  are  perceived  ;  3d,  when  the  foramen  ovale 
and  the  ductus  arteriosus  Botalli  are  both  open,  or,  indeed, 
only  the  latter  ;  4th,  when  the  opening  of  the  foramen  ovale 
is  proportionately  large,  the  ductus  being  closed,  and  especi- 
ally when  its  size  depends  on  want  of  the  fleshy  substance  of 
the  septum  ;  5th,  when  the  valves  of  the  pulmonary  artery 
show  anomalies  of  structure  that  are  evidently  congenital  ; 
6th,  when  the  trunk  of  the  pulmonary  artery  is  decidedly 
contracted  and  its  walls  are  too  thin  ;  7th,  when  the  right 
ventricle  appears  contracted  or  stunted.'^ 

The  appearances  which  are  met  with  in  congenital 
stenosis  differ  very  considerably  in  different  cases.  The 
most  common  condition  is  that  in  which  the  pulmonary 
artery  is  distinctly  differentiated  from  the  aorta,  and  narrowed 
or  completely  occluded.  In  cases  of  this  description  the  valve 
segments  may  be  fused  together,  or  irregular  in  development ; 
the  foramen  ovale  is  usually  patent,  the  ductus  arteriosus  is 
in  some  cases  open,  in  others  closed  ;  there  is  sometimes  a 
deficiency  in  the  intra-ventricular  septum. 

In  other  cases,  the  stenosis  is  chiefly  situated  in  the  right 
conus  arteriosus,  which  may  appear  to  be  a  third  ventricle  cut 
off  from  the  other  two.  In  cases  of  this  description  the  intra- 
ventricular septum  is  usually  deficient,  the  foramen  ovale 
usually  open,  the  ductus  arteriosus  sometimes  open,  sometimes 
closed.  The  trunk  of  the  pulmonary  artery  is  usually  con- 
stricted, and  the  coats  of  the  vessel  thinner  than  normal. 

In  a  third  group,  still  more  striking  anomalies  are  found. 
In  some  the  division  of  the  common  truncus  arteriosus  into 
the  pulmonary  artery  and  aorta  is  incomplete  ;  in  others,  in 
addition  to  the  stenosis  or  complete  occlusion  of  the  pulmonary 
artery,  the  heart  may  only  consist  of  two  cavities,  or,  there  may 
be  one  ventricle  and  two  auricles,  or  two  ventricles  and  one 
auricle  ;    in  others  again,  in  addition   to   the  stenosis  of  the 

'   Ziciusscii's  Cyclofadia,  vol.  vi.  p.  31S. 


544  Diseases  oj  the   Heart. 

pulmonary  artery,  the  aorta  and  pulmonary  arter}-  are  trans- 
posed, or  have  some  other  abnormal  connections  with  the  heart. 
The  appearances  which  the  pulmonary  orifice  presents  in 
cases  of  congenital  stenosis  are  beautifully  represented  in  figs. 
222  to  228,  which,  through  the  courtesy  of  his  executors,  I  am 
able  to  reproduce  from  the  late  Dr  Peacock's  great  work  On 
Malformation  of  the  Human  Heart. 

Patliological  physiology. — In  the  acquired  form  of  stenosis 
the  same  changes  are  observed  in  the  right  heart  and  pul- 
monary artery,  which  are  seen  in  the  left  heart  and  aorta  as 
the  result  of  aortic  stenosis  ;  in  both  cases  regurgitation  is 
very  generally  combined  with  constriction. 

The  right  ventricle  thus  becomes  hypertrophied  and  more 
or    less    dilated.     When    the    stenosis    is    considerable,    the 


Descr'qdlon  offys.  ti'l,  'li'd,  'li-i  and  'lib,  which  illustrutt  Coiutrictioii  of  the 
Pulmonary  Orifice.  (^Ajltr  Peacock.') 
Fig.  '2.i'2. — '  Diagram  to  show  the  extreme  coustrictiou  at  the  commencement  of 
the  conus  arteriosus,  the  atrophy  of  that  portion  of  the  ventricle,  and  the  form  of 
tlie  arterial  opening  in  Case  VIII.,  p.  ^\  (in  Dr  Peacock's  work  On  Malformation  of 
the  Human  Heart).  The  pulmonary  valves  are  only  two  in  number,  and  one  of  them 
displays  appearances  of  imperfect  division.  Tho  subject  of  the  disease  was  a  boy 
7  years  old. 

a,  Rudimentary  conus  arteriosus. 

b,  Piece  of  wood  passed  through  opening  in  septum  between  the  conus  and  tho 
sinus  of  the  right  ventricle.' 

Pig.  223  — Heart  in  Case  XIII.,  described  at  p.  112,  in  Dr  Peacock's  work 

On  Malformation  oftlie  Human  Heart. 

'  The  preparation  is  numbered  B  3  in  the  Museum  of  the  Victoria  Park  Hospital. 

The  septum  of  the  ventricles  is  entire,  yet  the  hypertrophy  of  the  right  ventricle  i.s 

seen  to  be  very  great.     The  young  man  who  was  the  subject  of  the  disea.se  died  at  the 

age  of  20. 

a.  The  right  ventricle  laid  open  to  show  the  great  hypertrophy  of  its  parietes. 
6,  The  pulmonic  orifice.' 

Fig.  224. — The  orifice  of  the  pulmonurij  artery  {Case  XIII.)  as  seen  from  aboie. 
'  The  union  of  the  three  valves  into  one,  the  frena  or  bands  which  mark  the  im- 
perfect division  of  the  segments,  the  thickening  of  the  whole  of  the  valves,  and  the 
form  of  the  orifice,  are  well  shown  in  this  drawing.     The  aperture  is  seen  also  to 
have  been  permanently  patent.' 

Fig.  225. — '  The  foramen  ovale  in  the  same  case,  showing  that  the  process  of 
closure  has  never  been  completed,  the  coruua  of  the  valve,  «,  «,  still  remaining  widely 
apart.' 


Fig. 222 


Fig.  225 


^ 


Fig.  224. 


Flos.  222,  223,  224,  and  225,  illustrate  Stenosis  of  the  Pulmonary  Orifice.    {After  Peacock.') 
For  description  see  page  544. 


Fig.  226. — Deficiency  in  the  neptum  ventricvhrum  from  a  fpecimen  exhibited  at  tht 
Patlwlofjical  iSociety,  by  iJr  Quaiti,  in  1S56. 

'The  preparation  was  takeu  from  a  youth  eigliteeu  years  of  age,  who  died  of 
phthisis  at  the  Bronipton  liospital,  under  the  care  of  Dr  Cursham.  He  liad  bten 
cyanotic  siuce  he  was  two  years  of  age.  Tlie  •  aperture  was  sufficiently  large  to 
permit  a  florin  to  pass  through,"  and  was  remarkable  for  occupying  the  whole  of  the 
undefended  .space  and  for  its  regular  triangular  form.' — (^On  Malformation  of  the 
Human  Heart,  by  Pr  Peacock,  p.  ol.) 


Fio.  227. 


Fig.  22a 


Nfly^gr- 


Fig.  it,  .—Constriction  of  tite  pulmonary  orifice.    {After  Peacock.') 

'  The  pulmonarj'  valves  are  united  so  as  to  form  an  infundibular  or  funnel-shape 
opening  from  the  ventricle  into  the  artery;  the  ductus  arteriosus  is  pervious  and 
the  foramen  ovale  open.'  ' 

Fig  228. — For  description  see  page  546. 


M<b«»(Ci/».M  Lnn>  EmS 


Co2trse  of  the  Blood  in  the  Foehis.  545 

pulmonary  circulation  is  imperfectly  supplied  with  blood  ; 
the  tricuspid  may  become  incompetent,  and  the  systemic 
venous  system  engorged.  Compensation  in  cases  of  this 
description  is  chiefly  effected  by  the  hypertrophy  of  the  right 
ventricle. 

In  congenital  cases,  the  secondary  results,  and  the  manner 
in  which  compensation  is  established,  vary  in  different  cases, 
and  depend  chiefly  upon  the  period  of  intra-uterine  life  at 
which  the  stenosis  of  the  pulmonary  artery  is  established. 

But  in  order  that  these  points  may  be  thoroughly  under- 
stood, it  is  necessary  to  remember  the  course  of  the  circulation 
during  intra-uterine  life.  It  is  represented  in  fig.  229,  and  is 
as  follows  : — 

'  Course  of  the  Blood  in  the  Fcctits. — The  right  auricle  of  the  foetal 
heart  receives  blood  from  the  two  vente  cavas  and  the  coronary  vein. 
The  blood  brought  by  the  superior  cava  is  simply  the  venous  blood 
returned  from  the  head  and  upper  half  of  the  body  ;  whilst  the  inferior 
cava,  which  is  considerably  larger  than  the  superior,  con\eys  not  onh' 
the  blood  from  the  lower  half  of  the  body,  but  also  that  which  is  returned 
from  the  placenta  and  from  the  liver.  This  latter  stream  of  blood 
reaches  the  vena  cava  inferior,  partly  by  a  direct  passage — the  ductus 
venosus — and  partly  by  the  hepatic  veins,  which  bring  to  the  vena  cava 
inferior  all  the  blood  circulating  through  the  liver,  whether  derived  from 
the  supply  of  placental  blood  entering  that  organ  by  the  umbilical  vein, 
or  proceeding  from  the  vena  portas  or  hepatic  artery. 

The  blood  of  the  superior  vena  cava,  passing  from  the  right  auricle 
into  the  right  ventricle,  is  thence  propelled  into  the  trunk  of  the 
pulmonary  artery.  A  small  part  of  it  is  distributed  through  the  branches 
of  that  vessel  to  the  lungs,  and  returns  by  the  pulmonary  veins  to  the  left 
auricle  ;  but  as  these  vessels  remain  comparatively  undilated  up  to  the 


Description  of  F'uj.  228. 
Contraction  of  the  outlet  of  the  rirjht  ventricle  men  from  above.  (^After  Peacock.') 
The  constriction,  which  was  very  great,  was  situated  at  the  base  of  the 
pulmonary  cusps,  and  was  formed  by  a  muscular  band  covered  by  iibrous  tissue;  the 
edges  of  the  opening  were  studded  with  warty  vegetations  Immediately  beyond  the 
constriction  the  passage  expanded,  so  that  the  valves  themselves  freely  admitted  the 
forefinger  between  them.  The  segments  were  two  in  number,  and  one  of  them  dis- 
played some  remains  of  a  frenum  or  band  on  the  upper  surface.  Except  being  some- 
what thickened  and  opaque,  they  were  free  from  disease.  There  was  a  deejj  sinus 
behind  each  of  them  The  pulmonary  artery  was  of  small  size. — For  further  descrip- 
tion of  the  case,  see  Dr  Peacock's  work  On  Malformation  of  the  Hunmii  Heart,  p.  55. 

M    M 


546 


Diseases  of  the   Heaif. 


Fig.  229. — Diagrammatic  outline  of  the  organs  of  circulation  in  the  fa-tus  of 
six  months.     {After  Quain,  slighty  modified. ) 

RA,  right  auricle  of  the  heart ;  RV,  right  ventricle  ;  LA,  left  auricle  ;  Ev, 
eustachian  valve  ;  LV,  left  ventricle  ;  L,  liver  ;  K,  left  kidney  ;  I,  portion  of 
small  intestine  ;  a,  arch  of  the  aorta  ;  a',  its  dorsal  part  ;  a",  lower  end  ;  vcs, 
superior  vena  cava  ;  vci,  inferior  vena  where  it  joins  the  right  auricle  ;  vci',  its 
lower  end  ;  s,  subclavian  vessels  ;  J,  right  jugular  vein  ;  c,  common  carotid 
arteries  ;  four  curved  arrow  lines  are  carried  through  the  aortic  and  pulmonary- 
opening,  and  the  auriculo-ventricular  orifices  ;  da,  opposite  to  the  one  passing 
through  the  pulmonary  arter)-,  marks  the  place  of  the  ductus  arteriosus  ;  a  similar 
arrow  line  is  shown  passing  from  the  vena  cava  inferior  through  the  fossa 
ovalis  of  the  right  auricle,  and  the  foramen  ovale  into  the  left  auricle  ;  hv,  the 
hepatic  veins  ;  vf,  vena  portse  ;  x  to  vci,  the  ductus  venosus  ;  uv,  the  umbilical 
vein  ;   ua,  umbilical  arteries  ;  uc,  umbilical  cord  cut  short  ;  /  i' ,  iliac  vessels. 


Patholoo-y  of  Piihuonary  Stejiosis.  547 

time  of  birth,  by  far  the  larger  part  passes  through  the  ductus  arteriosus 
into  the  dorsal  aorta,  and  is  thence  distributed  in  part  to  the  lower  half 
of  the  body  and  the  viscera,  and  in  part  is  conveyed  along  the  umbilical 
arteries  to  the  placenta.  From  these  several  organs  it  is  returned  by 
the  vena  cava  inferior,  the  venae  portae,  and  the  umbilical  vein  ;  and,  as 
already  noticed,  reaches  the  right  auricle  through  the  trunk  of  the 
inferior  cava. 

Of  the  blood  entering  the  heart  by  the  inferior  \  ena  ca\a,  only  a  small 
part  is  mingled  with  that  of  the  superior  cava,  so  as  to  pass  into  the  right 
ventricle  ;  by  far  the  larger  portion,  directed  by  the  Eustachian  valve 
through  the  foramen  ovale,  flows  into  the  left  auricle,  and  thence, 
together  with  the  small  quantity  of  blood  returned  from  the  lungs  by  the 
pulmonary  veins,  passes  into  the  left  ventricle,  from  whence  it  is  sent 
into  the  arch  of  the  aorta,  to  be  distributed  almost  entirely  to  the  head 
and  upper  limbs. 

Sabatier  was  the  first  to  call  attention  particularly  to  the  action  of  the 
Eustachian  valve  in  separating  the  currents  of  blood  entering  the  right 
auricle  by  the  superior  and  inferior  venae  cavas.  This  separation,  as 
well  as  that  occurring  between  the  currents  passing  through  the  aortic 
arch  and  the  ductus  arteriosus  into  the  descending  aorta,  was  illus- 
trated experimentally  by  John  Reid.  A  striking  confirmation  of  the  ex- 
tent to  which  the  last  mentioned  division  of  the  two  currents  of  the  foetal 
blood  may  take  place,  without  disturbance  of  the  circulation  up  to  the 
time  of  birth,  is  afforded  by  the  examples  of  malformation  in  which  a 
complete  obliteration  has  existed  in  the  aortic  trunk  immediately  before 
the  place  of  the  union  of  the  ductus  arteriosus  with  the  posterior  part  of 
the  aortic  arch.'i 

Now  when  the  stenosis  of  the  pulmonary  artery  is  pro- 
duced before  the  end  of  the  third  month  of  intra-uterine  hfe, 
i.e.  before  the  separation  of  the  two  ventricles  is  completed, 
the  intra-ventricular  septum  remains  imperfect,  the  aperture 
between  the  two  ventricles  being  a  round  hole  with  smooth 
edges.  In  cases  of  this  description,  the  blood,  which  ought  to 
pass  after  birth  from  the  right  ventricle  through  the  lungs  to 
the  left  ventricle,  makes  its  way  directly,  i.e.  by  a  short  cut 
from  ventricle  to  ventricle  through  the  aperture  in  the  intra- 
ventricular septum.  The  blood  finds  its  ways  to  the  lungs 
either  through  the  ductus  arteriosus,  or,  if  as  is  frequently  the 
case,  that  vessel  is  closed,  through  some  branches  of  the 
aorta  (usually  the  bronchial,  oesophageal,  anterior  coronary  or 

'   (^uain  s  Anatomy,  ninth  edition,  vol.  ii.  p.  875. 


548  Diseases  of  the   Heart. 

pericardial  arteries),  inosculating  with  branches  of  the  pul- 
monary arteries. 

When  the  lesion  is  produced  after  the  third  month,  the 
intra-ventricular  septum  is  closed,  and  compensation  is  effected 
by  the  foramen  ovale  remaining  patent.  After  birth,  the 
blood,  instead  of  passing  from  the  right  ventricle  through  the 
lungs  to  the  left  heart,  passes  directly  from  the  right  to  the 
left  auricle  ;  the  lungs  are  supplied  with  blood  either  through 
the  ductus  arteriosus  remaining  patent,  or,  if  that  vessel  is 
closed,  through  the  inosculation  between  branches  of  the  aorta 
and  the  pulmonary  artery. 

In  both  groups  of  cases,  the  compensation  is  seldom 
perfect,  the  superficial  veins  are  usually  enlarged,  and  more  or 
less  cyanosis  is  generally  present.  The  balance  of  compensa- 
tion, too,  is  easily  upset,  any  slight  pulmonary  affection,  for 
example,  causing  a  great  increase  in  the  cyanosis  and  other 
symptoms. 

The  condition  of  the  right  ventricle  varies  in  different  cases, 
in  some  it  is  markedly  hypertrophied  ;  in  others,  as  for 
instance  in  those  cases  in  which  the  orifice  is  completely 
occluded,  it  may  be  much  smaller  than  normal  or  quite 
rudimentary.  The  lungs  are  usually  found  to  be  anaemic ;  and 
in  cases  which  live  to  the  age  of  puberty,  chronic  tubercular 
changes  in  the  lungs  are  extremely  frequent,  and  are  in  a  large 
proportion  of  cases  the  immediate  cause  of  death. 

Ctinical  History. — It  is  unnecessary  to  give  a  separate  de- 
scription of  the  acquired  and  congenital  forms  of  the  disease, 
for  the  symptoms  in  acquired  cases  are  identical  with  the 
symptoms  in  some  of  the  congenital  cases  in  which  the  lesion 
is  not  severe,  and  in  which  the  symptoms  do  not  develop  until 
later  life.  We  may  conveniently  divide  cases  of  congenital 
stenosis  of  the  pulmonary  artery  into  three  clinical  groups  or 
types,  viz. : — 

First  group. — Cases  in  zvhich  the  lesion  is  very  severe,  and 
in  wJiieh  the  patient  dies  immediately,  or  soon  after  birth. 

In  the  most  severe  cases  of  this  description,  the  child  dies 
asphyxiated    immediately  after  birth  ;    in   some   cases,  life  is 


Clinical  History  of  Puliiiouary  Stenosis.'       549 

beolonged  for  a  few  weeks  or  months ;  cyanosis  is  very 
prominent,  and  is  very  much  increased  by  anything,  as  for 
instance  coughing  or  crying,  which  further  embarrasses  the 
lungs  or  right  heart  ;  the  temperature  is  usually  subnormal ; 
somnolence  is  a  characteristic  symptom,  in  one  case,  for 
instance,  which  came  under  my  own  observation,  the  child 
would  sleep  for  eighteen  or  twenty-four  hours  at  a  stretch  ; 
dropsy  of  the  feet  may  develop  ;  shortness  of  breath  and 
pulmonary  complications  are  often  present  ;  convulsions  are 
not  uncommon. 

Second  group. — Cases  in  zvJiicJi  the  lesion  is  less  severe,  and 
in  ivhich  life  may  be  prolonged  for  several  years,  bnt  in  tvhich 
there  aj-e  from  the  first,  symptoms  indieative  of  the  cardiac 
lesion. — In  cases  of  this  description  there  is  more  or  less 
cyanosis,  which  may  however,  only  be  noticeable  on  cough- 
ing, crying,  etc.,  or  when  the  right  heart  and  pulmonary 
circulation  become  embarrassed  by  any  sudden  effort,  attacks 
of  bronchitis  or  other  lung  complications;  the  blueness  is 
most  noticeable  in  the  peripheral  parts  of  the  body;  the 
fingers  are  clubbed  ;  the  superficial  veins  are  usually  promi- 
nent ;  the  child  develops  slowly,  and  looks  much  younger 
than  his  years ;  shortness  of  breath  on  exertion,  and 
palpitation  are  generally  prominent  symptoms  ;  pulmonary 
complications,  such  as  attacks  of  bronchitis  and  haemoptysis 
are  frequent  ;  headache,  giddiness,  or  even  epileptiform 
convulsions  (the  result  of  deranged  cerebral  circulation)  are 
sometimes  seen.  Dropsy  is  seldom  present  in  cases  of  this 
description  until  the  failure  of  compensation,  or  unless  the 
venous  circulation  becomes  suddenly  much  embarrassed  by 
intercurrent  complications,  such  as  acute  bronchitis,  acute 
endocarditis,  etc.  Children  affected  in  this  manner  are  very 
susceptible  to  cold  and  all  injurious  external  influences  ;  their 
mental  development  may  be  retarded  ;  and  if  they  survive  the 
trying  ordeal  of  puberty,  they  are  very  apt  to  die  in  early 
manhood — between  the  ages  of  fifteen  and  twenty-five — from 
phthisis  ;  the  lung  disease,  as  a  rule,  runs  a  protracted  course, 
the  left  lung  is  usually  the  first  to  be  attacked,  and  repeated 
haemorrhage  is    commonl)-  observed.       In    exceptional    cases 


550  Diseases  of  iJte  Heart. 

included  under  this  group,  life  may  be  prolonged  for  years. 
Lebert,  for  example,  mentions  that  in  one  case  of  undoubted 
congenital  stenosis,  the  patient  attained  the  age  of  sixty-five 
years.^ 

Third  group. — Cases  in  ivliich  the  lesion  is  slight. — In  cases  of 
this  description,  the  usual  symptoms  of  congenital  heart  disease 
may  be  slight  or  entirely  absent.  Years  after  birth  cyanosis 
and  shortness  of  breath  and  the  other  indications  of  a  right- 
sided  lesion  ma}-  arise,  and  are  usually  due  either  to  the  failure 
of  compensation,  which  has  hitherto  been  perfect,  or  to  the 
occurrence  of  acute  endocarditis,  bronchitis  or  some  other 
pulmonary  complication.  When  the  pulmonar\-  stenosis  is 
acquired  the  same  s}'mptoms  ma)'  arise. 

Physical  signs. — In  cases  of  acquired  pulmonary  stenosis 
the  ph}'sical  signs  arc: — (i)  A  .systolic  murmur  having  its  point 
of  differential  maximum  intensity  in  the  second  left  interspace. 


Fig.   230. — Outline  figure  showing  the  ])oint  of  difterential  inaxiniuni  intensity  of 
the  systolic  puhnonary  murmur,  and  tlie  direction  in  which  it  is  propagated. 

'  Ziemsseti's  Cyc/o/,cdia.  vol.  vi.  p.  317. 


Physical  Signs  of  Pulmonary  Stenosis.         551 

or  at  the  junction  of  the  third  left  costal  cartilage  with  the 
sternum,  and  its  direction  of  propagation  upwards  and  towards 
the  left  (see  fig.  230).  The  murmur,  which  is  in  some  cases 
loud  and  harsh  in  others  soft  and  faint,  is  not  heard  in  the 
carotids  ;  a  thrill  can  in  some  cases  be  felt  over  the  position 
of  the  murmur.  (2)  A  faint  or  inaudible  pulmonary  second 
sound  ;  in  those  cases  in  which  the  valve  is  incompetent  as 
well  as  stenosed,  a  diastolic,  as  well  as  the  systolic  murmur,  is 
present.  (3)  Increased  dulness  over  the  right  heart,  and  the 
usual  indications  of  right-sided  hypertrophy  and  dilatation. 
(4)  Fulness  of,  and  in  some  cases  pulsation  in,  the  superficial 
veins,  the  external  jugulars  for  example,  together  with  more 
or  less  cyanosis.  (5)  A  small  and  weak,  in  some  cases 
irregular  radial  pulse. 

In  congenital  cases,  a  systolic  murmur  can  generally  be 
heard  over  the  praecordial  region  ;  its  point  of  maximum 
intensity  varies  in  different  cases,  but  is  usually  situated  in  the 
second  and  third  left  interspaces  ;  in  many  cases  the  murmur 
is  a  loud  one,  and  may  be  heard  all  over  the  praecordia.  (The 
exact  significance  of  a  systolic  murmur  in  cases  of  congenital 
heart  disease  is  not  always  clear ;  in  some  it  is  probably  due 
to  fluid  veins  formed  as  the  blood  passes  through  the  con- 
stricted pulmonary  orifice  ;  in  cases  of  this  description  the 
pulmonary  second  sound  is  feeble,  altogether  absent,  or  replaced 
by  a  diastolic  murmur  ;  in  others  it  is  probably  produced  b}' 
the  passage  of  the  blood  through  the  patent  foramen  ovale  or 
through  an  aperture  in  the  intra-ventricular  septum  ;  in  others, 
again,  it  is  the  result  of  mitral  or  tricuspid  regurgitation.^) 

A  systolic  thrill  can  in  some  cases  be  felt  over  the  region  of 
the  murmur.  When  the  right  ventricle  is  enlarged,  as  it  is  in 
many  cases,  increased  dulness  over  the  region  of  the  right  heart 
and  (in  some  cases)  bulging  of  the  praecordial  region  are 
present.- 

'   In  this  case  the  murmvir  would  be  presystolic  rather  than  systolic. 

-  The  right  ventricle  is  not  hypertrophied  or  dilated  in  all  cases  of  congenital 
stenosis  of  the  pulmonary  artery.  When,  for  example,  the  occlusion  is  complete 
it  may  be  smaller  than  normal  ;  when,  again,  the  intra-ventricular  septum  is 
imperfect,  there  may  be  no  alteration  in  the  size  of  the  right  heart, 


552  Diseases  of  tlic  Heart. 

The  superficial  veins  are  usually  prominent,  and  in  some 
cases  pulsate  ;  the  radial  pulse  is  (as  a  rule)  small  and  weak. 

Diagnosis.— V<l\\Q^n  a  systolic  murmur  is  heard  over  the 
region  of  the  pulmonary  artery  we  have  to  inquire : — 

(i)  Is  the  murmur  actually  produced  in  the  pulmonary 
artery  ? 

(2)  If  the  murmur  is  produced  in  the  pulmonary  artery, 
is  it  due  to  functional  conditions  (such  as  auctmia)  or  to 
organic  disease  {i.e.  stenosis  of  the  orifice)  ? 

(3)  If  organic,  is  it  congenital  or  acquired  ? 

Further,  in  all  cases  of  cyanosis  and  congenital  heart 
disease,  whether  a  systolic  pulmonary  murmur  is  present  or 
not,  we  have  to  inquire  whether  the  case  is  one  of  stenosis 
or  complete  occlusion  (atresia)  of  the  pulmonary  artery. 

Step  No.  I.  Is  the  vmruiur  produced  in  the  pulmonary 
artery? — A  pulmonary  systolic  murmur  can  usually  be  distin- 
guished from  other  systolic  endocardial  murmurs  (viz.,  from 
systolic  aortic,  tricuspid,  and  mitral  murmurs),  by  observing 
its  point  of  differential  maximum  intensity,  its  direction  of 
propagation,  the  size  and  shape  of  the  right  and  left  hearts, 
and  the  condition  of  the  peripheral  venous  and  arterial 
circulations.     (See  Table  VIII.,  p.  527.)^ 

Step  No.  2.  If  the  murmur  is  produced  in  tJie  pulmonary 
artery,  is  it  due  to  functional  derangement  or  to  organic 
disease  ?  —  Functional  (haemic)  murmurs,  which  are,  as 
we  have  previously  seen,  very  frequently  indeed  heard  in 
the  pulmonary  area,  can  usually  be  distinguished  from 
pulmonary  murmurs  due  to  organic  disease  {i.e.  stenosis 
of  the  pulmonary  orifice)  by  attention  to  the  following 
points  : — 

I.  The  colour  of  the  skin  and  mucous  Diembrancs. — When 
the  murmur  depends  on  anaemia,  the  skin  and  mucous 
membranes  are  of  course  pale,  and  the  other  indications 
of    anaemia    are    present.       On    the    other   hand,   when    the 

'  Naunyn,  Balfour,  and  others,  believe  thai  a  mitral  systolic  murmur  is  some- 
times heard  in  the  second  left  interspace  rather  than  at  the  apex  of  the  heart. 
This  point  is  fully  considered  on  p.  190, 


Diagnosis  of  Piilinoiiai'y  Stenosis.  553 

murmur  is  due  to  organic  disease,  i.e.  stenosis  of  the  valvular 
orifice,  the  patient  is  more  or  less  cyanotic. 

2.  The  nature  of  tJie  symptoms. — When  the  murmur  is 
due  to  anaemia,  lung  symptoms  and  the  signs  of  venous 
engorgement  are  not  prominent.  In  organic  stenosis,  on  the 
contrary,  cough,  shortness  of  breath,  even  when  at  rest, 
dropsy,  and  the  other  symptoms  and  signs  of  venous  en- 
gorgement, may  be  very  prominent. 

3.  TJie  conditio)i  of  tJie  right  heart. —  In  anaemia  there  is 
usually  some  enlargement  (hypertrophy  and  dilatation)  of 
the  right  heart,  but  it  is  never  extreme  ;  in  organic  stenosis, 
on  the  contrary,  the  enlargement  of  the  right  heart  (both 
ventricle  and  auricle)  may  be  great. 

4.  A  venous  Juim  in  the  neek  is  present  in  anaemia,  but  (.-') 
not  in  organic  stenosis. 

5.  T/ie  character  of  the  pntse. — In  the  earlier  stages  of 
anaemia,  the  pulse  is  of  good  tension,  but  very  irritable  and 
variable  in  rate  ;  in  organic  stenosis,  the  radial  pulse  is 
small,  weak,  and  may  be  intermittent. 

6.  The  character  of  the  pulmonary  second  sound. — Always 
present  and  usually  accentuated  in  anaemia ;  faint,  absent 
or  replaced  by  a  diastolic  murmur  in  organic  stenosis. 

7.  The  effects  of  treatment. — Anaemia  and  its  attendant 
pulmonary  murmur  are,  with  rare  exceptions  (some  cases  of 
progressive  pernicious  anaemia)  completely  and  speedily  cured 
by  appropriate  treatment ;  organic  stenosis  is  incurable. 

This  seems  an  appropriate  place  to  refer  to  a  peculiar 
loud  systolic  murmur  which  is  heard  over  the  situation  of 
the  pulmonary  artery  in  some  cases  in  which  the  left  lung 
is  retracted.  Quincke,  who  first  described  this  murmur, 
supposed  that  it  is  produced  by  the  pulmonary  artery  being 
constricted  by  the  pressure  of  the  heart  during  the  contrac- 
tion of  the  ventricles.  In  the  cases  in  which  the  murmur 
is  audible,  the  pulsation  of  the  pulmonary  artery  can  be 
seen  and  felt  in  the  second  left  interspace.  A  peculiar 
feature  about  this  murmur  is  that  it  disappears  during  a  full 
inspiration,  that  is  when  the  pulmonary  artery  is  covered  and 


554  Diseases  of  t lie  Heart. 

separated  from  the  chest  wall  by  the  fully  expanded  lung. 
Dr  G.  Balfour,  in  his  Clinical  Lectures  on  the  Diseases  of  the 
Heart,  gives  the  details  of  several  cases  in  which  a  murmur 
of  this  description  was  present,  and  states  that,  '  though 
these  cases  cannot  be  held  to  have  proved  the  correctness  of 
Quincke's  theory,  they  yet  lend  a  very  strong  support  to  it.'^ 
Two  cases,  which  seemed  to  be  of  a  similar  nature,  have  come 
under  my  own  observation,  and  in  them  I  came  to  the  con- 
clusion that  the  murmur  was  exocardial,  and  produced  by  the 
contact  of  the  pulmonary  artery,  or  rather  the  roughened 
portion  of  the  pericardium,  which  covers  the  root  of  the 
pulmonary  artery,  with  the  anterior  wall  of  the  chest.  (In 
the  two  cases  to  which  I  refer  the  retraction  of  the  lung 
was  due  to  pleurisy,  and  there  was  every  reason  to  suppose 
that  the  outer  surface  of  the  pericardium  was  roughened  by 
a  deposit  of  lymph).  '  The  very  peculiar  loudness,  roughness, 
and  localised  character— not  propagated  in  any  direction — of 
the  murmur'  (to  quote  Dr  Balfour's  description  of  it)  seem 
to  me  to  lend  support  to  this  view  ;  while  it  is,  I  think,  ex- 
tremely doubtful  whether  the  heart  does  or  can  compress  the 
pulmonar)'  artery  in  the  manner  which  Quincke  has  supposed. 
Recent  observations  indeed  show  that  the  conus  arteriosus 
descends  to  the  plane  of  the  base  during  the  ventricular 
systole  ;  and  that  the  length  of  the  ventricle  does  not  alter 
during  the  contraction  of  the  heart.- 

Before  leaving  the  subject  of  pulmonary  murmurs,  I  must 
also  add,  on  the  authority  of  Dr  Hilton  Fagge,  and  I  can 
from  personal  observation  confirm  his  statement,  '  that  in 
children  (even  when  in  good  health)  a  murmur  over  the 
pulmonary  valves  may  be  generated  by  the  pressure  of  the 
stethoscope,  as  is  shown  by  the  fact  that  it  disappears  when 
the  instrument  is  lightly  applied.  It  is  said  that  a  similar 
murmur  has  sometimes  been  observed  even  in  adults,  when 
the  chest  walls  are  thin  and  yielding.'^ 

Step.  No.  3.- — If  the  murunir  is  produeed  in  the  pulmonary 

'   Diseases  0/  the  Heart,  p.  225. 

-   Macalibter,  British  Medical  Journal,  Oct.  28,  1S82,  ji.  S22. 

^   Russell  Reynold's  System  of  Medecine,  vol.  iv.  p.  639. 


Diagnosis  of  Piiliuonary  Stenosis.  555 

artery,  is  it  congaiital  or  acquired? — It  is  impossible  in  some 
cases  to  come  to  a  definite  conclusion  on  this  point,  for, 
as  we  have  previously  seen,  it  occasionally  happens  that 
a  congenital  lesion  of  the  pulmonary  artery  remains  entirely 
latent  for  some  years,  and  is  not  attended  by  any  symptoms 
until  several,  it  may  be  many  years,  after  birth.  In  cases 
of  this  description,  it  might  easily  be  supposed  that  the  lesion 
was  an  acquired  one  ;  in  fact,  in  many  cases  this  is  actually 
the  fact,  as  for  example  in  those  cases  in  which  the  con- 
genitally  malformed  valve  is  subsequently  attacked  by  acute 
or  subacute  endocarditis.  On  the  other  hand,  it  should  be 
remembered  that  cases  of  acquired  stenosis  of  the  pulmon- 
ary artery  are  extremely  rare.  The  differential  diagnosis  of 
acquired  and  congenital  stenosis  of  the  pulmonary  artery 
is,  therefore,  to  be  determined  by  making  a  careful  inquiry 
into  the  history  of  the  case.  Cyanosis,  shortness  of 
breath,  attacks  of  bronchitis  in  early  life,  are  very  strongly 
in  favour  of  the  congenital  variety.  The  family  history 
should  be  inquired  into,  for  it  is  not  uncommon  to  find 
several  members  of  one  family  dying  from,  or  affected  with 
congenital  heart  disease.  It  is  only  w^hen  the  symptoms 
and  signs  of  cardiac  disease  have  been  entirely  absent  in  early 
life  that  the  diagnosis  of  acquired  pulmonary  stenosis  can  be 
entertained. 

Tlie  differential  diagnosis  of  congenital  heart  disease  (e.g. 
pulmonary  stenosis),  primary  lung  disease  (e.g.  cirrhosis,  chronic 
bronchitis,  and  emphysema),  and  mitral  stenosis. 

All  of  these  conditions  may  be  attended  with  marked 
cyanosis,  enlargement  of  the  right  heart,  tricuspid  incompe- 
tence, and  the  usual  symptoms  and  signs  of  systemic  venous 
engorgement  ;  in  all  of  them  pulmonary  symptoms  and 
signs,  and  attacks  of  bronchitis  and  emphysema  may  be 
prominent,  and  it  may  require,  therefore,  great  care  and  dis- 
crimination to  arrive  at  a  correct  conclusion  as  to  the  exact 
nature  of  the  case. 

Pulmonary  stenosis  {i.e.  congenital  heart  disease)  can 
usually  be  differentiated  from  the  other  two  {i.e.  primary  lung 


556  Diseases  of  iJie  Heart. 

disease  and  mitral  stenosis)  by  a  careful  ph\'sical  examination 
and  inquiry  into  the  history  of  the  case.  In  pulmonary 
stenosis,  a  pulmonary  systolic  murmur  is  usually  present,  and 
the  second  sound  is  faint,  entirely  absent,  or  replaced  by  a 
diastolic  murmur  ;  whereas  in  mitral  stenosis  and  primary  lung 
disease,  there  is  no  systolic  pulmonary  murmur,  and  the  second 
pulmonary  sound  is  loudly  accentuated.^ 

In  the  majority  of  cases  of  pulmonary  stenosis,  a  history 
of  a  shortness  of  breath  and  more  or  less  cyanosis  from  the 
time  of  birth  can  be  elicited.  (A  history  of  cyanosis  and 
shortness  of  breath,  from  early  childhood  is  not,  however,  con- 
clusive evidence  of  congenital  heart  disease.)  I  have  known  a 
case  of  marked  cyanosis,  with  secondary  hypertrophy  and 
dilatation  of  the  right  heart,  and  eventually  tricuspid  regurgi- 
tation and  dropsy,  in  which  these  symptoms  dated  back  from 
childhood,  and  in  which,  therefore,  the  history  of  the  case 
was  suggestive  of  congenital  heart  disease.  In  cases  of  this 
description  reliance  must  chiefly  be  placed  upon  the  condition 
of  the  heart  as  elicited  by  physical  examination.  In  cases 
of  congenital  heart  disease,  cyanosis  is  usually  much  more 
prominent  than  dropsy,  whereas  in  mitral  stenosis  the  reverse 
is  the  case.  The  differential  diagnosis  of  mitral  stenosis  and 
of  primary  lung  disease,  with  secondary  changes  in  the  right 
heart,  is  in  some  cases  extremely  difficult.  The  manner  in 
which  a  decision  is  to  be  arrived  at,  has  been  previously 
described.     (See  p.  494.) 

Prognosis. — In  the  great  majority  of  cases  of  congenital 
stenosis  of  the  pulmonary  artery,  the  patient  dies  soon  after 
birth  ;  and  even  those,  who  attain  the  age  of  puberty,  usually 
succumb  during  early  adult  life,  tuberculosis  of  the  lungs 
being  a  very  frequent  cause  of  death.  Some  few  cases  live  to 
middle  life,  and  one  case  has  been  already  referred  to,  in  which 
the    patient    reached  the   advanced   age   of  sixty-five.-     The 

'  In  complete  atresia  there  may  be  no  pulmonary  systolic  murmur,  but  cases  of 
complete  occlusion  so  rarely  survive,  and  even  if  they  do  survive,  they  are  attended 
with  such  prominent  symptoms,  continuously  from  the  time  of  birth,  that  they 
could  hardly  give  rise  to  difficulties  in  diagnosis. 

■   Lebert,  Zic'insseii's  Cyclopicdia,  vol.  vi.  p.  317. 


Treatment  of  Piiliuonary  Stenosis.  557 

prognosis  is,  of  course,  most  unfavourable  in  those  cases  in 
which  the  cyanosis  is  severe.  The  acquired  form  is  so  ex- 
tremely rare,  that  it  is  hardly  possible  to  lay  down  any  general 
rule  as  to  the  duration  and  chances  of  life  ;  each  individual 
case  must  be  judged  on  its  own  merits,  taking  into  account  the 
severity  of  the  symptoms,  the  extent  of  the  secondary  de- 
rangements in  the  heart  and  circulation,  and  the  many  other 
considerations  which  have  been  detailed  under  the  head  of 
the  various  forms  of  chronic  valvular  lesions. 

Treatment. — Children  affected  with  congenital  heart  disease 
must  be  carefully  protected  from  cold  and  other  injurious 
external  influences  ;  anything  which  increases  the  cyanosis 
{i.e.  the  embarrassment  of  the  right  heart  and  venous  circu- 
lation, and  interferes  with  the  action  of  the  lungs)  such  as 
sudden  efforts,  must  be  rigidly  prohibited  ;  and  the  therapeutic 
measures  recommended  for  the  treatment  of  chronic  valvular 
lesions  of  the  left  heart,  must  be  carried  out  in  accordance 
with  the  requirements  of  each  special  case. 

PULMONARY   INCOMPETENCE. 

^tiotflgj'. — Pulmonary  regurgitation  is  extremely  rare  :  it 
is  occasionally  met  with  as  a  congenital  condition,  and  is  then 
generally  combined  with  pulmonary  stenosis.  In  extremely 
rare  cases,  pulmonary  incompetence  is  produced  after  birth 
in  the  course  of  ulcerative  endocarditis.  It  hardly  ever  re- 
sults from  the  simple  form  of  endocarditis  or  atheromatous 
changes.  Theoretically  we  might  suppose  that  '  relative'  in- 
competence of  the  pulmonary  valves  might  be  caused  by 
over-distention  and  dilatation  of  the  pulmonary  artery,  but, 
as  a  matter  of  fact,  the  dilatation  of  the  vessel  is  seldom,  if 
ever,  sufficiently  great  to  interfere  with  the  perfect  closure  of 
the  valve  flaps. 

Pathotogical  physiology. — The  effect  of  pulmonary  regur- 
gitation would,  of  course,  be  to  allow  a  certain  quantity  of 
blood,  which  ought  to  be  retained  in  the  pulmonary  artery 
and   lungs,  to   pass   backwards    into   the   cavity  of  the   right 


55^  Diseases  of  tJic  Heart. 

ventricle  during  the  ventricular  diastole.  As  in  aortic  incom- 
petence, hypertrophy  and  more  especially  dilatation  of  the 
right  ventricle,  would  result ;  this  would  ultimately  be  fol- 
lowed by  relative  incompetence  of  the  tricuspid,  and  the 
usual  symptoms  and  signs  of  systemic  venous  engorgement. 
In  congenital  cases,  the  incompetence  is  usually,  as  I  have 
already  mentioned,  combined  with  stenosis  ;  and  in  cases  of 
this  description,  the  foraman  ovale  remains  open,  and  the 
extreme  engorgement  of  the  systemic  \enous  circulation  is 
thereby  relieved. 

Clinical  History. — In  congenital  cases,  the  symptoms  are 
identical  with  those  of  pulmonary  stenosis.  In  those  cases  in 
which  the  lesion  is  due  to  ulcerative  endocarditis,  symptoms 
and  signs  of  rapid  embarrassment  of  the  right  heart,  of  embolic 
infarctions  in  the  lungs  and  other  pulmonary  lesions,  and  of 
engorgement  of  the  systemic  venous  circulation,  together  with 
the  grave  constitutional  symptoms  which  characterise  ulcera- 
tive endocarditis  (see  page  406)  would  be  present.  In  those 
infinitely  rare  cases,  in  which  pulmonary  regurgitation  is  slowly 
and  gradually  established  after  birth,  secondary  changes,  more 
especially  hypertrophy  of  the  right  ventricle,  may  for  a  time 
compensate  the  lesion.  Shortness  of  breath,  cough,  and  other 
indications  of  pulmonary  derangement  would  probably  be 
present  through  the  stage  of  compensation.  Sooner  or  later 
the  tricuspid  would  give  way,  and  the  symptoms  due 
to  engorgement  of  the  venous  systemic  circulation  would 
develop. 

Physical  signs. — Pulmonary  incompetence  is  attended 
with  a  diastolic  murmur,  which  has  its  point  of  differential 
maximum  intensity  in  the  pulmonary  area,  and  its  direction 
of  propagation  downwards  and  towards  the  right.  The  mur- 
mur, like  the  diastolic  murmur  of  aortic  regurgitation,  would 
probably  in  many  cases  be  best  heard  at  the  lower  end  of  the 
sternum.  The  usual  physical  signs  indicative  of  hypertrophy 
and  dilatation  of  the  right  heart  are  also  present.  The  venous 
system  is  engorged,  the  arterial  system  empty,  the  pulse  being 
small,  weak,  and  probably  irregular. 


Diagnosis  of  Pitlnionary  IncoDipeteJicc.  559 

Diagnosis. — The  diastolic  murmur  indicative  of  pulmonary 
incompetence  might  be  readily  mistaken  for  the  diastolic 
murmur  of  aortic  regurgitation,  since  the  latter  is  so  common, 
the  former  so  rare.  The  points  of  distinction  between  the  two 
conditions  are  given  in  the  following  table  : — 

Table  IX.  —  TJie  Differential  Diagnosis  of  the  Diastolic 
of  Aoftic  Murmurs  and  Pulmonary  Incompetence. 

Aortic  Incompetence.        Pulmonary  Incompe- 
tence. 

Point  of  differential  niaxi-     Second    right    costal    car-     Second  left  interspace,  or 
imim    intensity    of   tJie         tilage.  third  left  cartilage. 

murmnr. 

Direction    of  propagation     Downwards    and    to    the     Downwards   and    to    the 


of  miirmiir. 
Condition  of  left  ventricle. 


Condition    of   right    ven- 
tricle. 


left. 

Dilated  and  hypertro- 
phied. 

Normal  (unless  some  com- 
plication, such  as  second  - 
ary  rnitral  incompe- 
tence. ) 


right. 

Normal       (unless       some 
complication). 

Hypertrophied    and    dila- 
ted. 


Condition   of  radial   and    Jerking, visible, collapsing,     Small,    weak,    and    often 


otlier  superficial  pnlsts. 
Condition  of  venous  system. 


Condition    of  pidmonary 
circulation. 


irregular. 

Engorged,  often  extreme- 
ly so,  and  all  the  usual 
results  of  venous  ob- 
struction, such  as 
dropsy,  present. 

Distended  during  the  ven- 
tricular systole,  empty 
during  diastole  ;  pul- 
monary symptoms  usu- 
ally prominent. 

Prognosis. — Unfavourable  as  regards  the  ultimate  result, 
though  Rosenstein  states  that  '  if  we  may  draw  conclusions 
from  the  exceedingly  limited  number  of  cases  on  record,  the 
length  of  the  patient's  life   .    .    .   may  be  comparatively  long.' ^ 


Normal  (unless  some  com- 
plication such  as  second- 
ary mitral  incompe- 
tence). 

Normal  (unless  some  com- 
plication, such  as  second- 
ary mitral  incompe- 
tence). 


Treatment. — In  the  earlier  stages  of  the  case,  the  same  treat- 
ment which  has  been  recommended  for  aortic  regurgitation 
(see  519)  should  be  adopted;  after  venous  engorgement 
becomes  prominent  the  treatment  suitable  for  mitral  lesions  is 
to  be  employed. 

'  Zienissen's  Cyclopcrdia,  vol.  vi.  p.  155. 


560  Diseases  of  the  Heart. 


CHAPTER    VI. 

DISEASES  OF  THE  MYOCARDIUM.  ACUTE  MYOCARDITIS.  CHRONIC  MYO- 
CARDITIS OR  FIBROID  DEGENERATION.  PARTIAL  ANEURISMS  OF 
THE  HEART.  HYPERTROPHY  AND  DILATATION  HYPERTROPHY  OF 
THE  LEFT  VENTRICLE.  HYPERTROPHY  OF  THE  RIGHT  VENTRICLE. 
HYPERTROPHY  OF  THE  AURICLES.  ATROPHY  OF  THE  HEART 
FATTY  INFILTRATION.  FATTY  DEGENERATION.  SPONTANEOUS 
RUPTURE.     TUMOURS  OF  THE  HEART. 

The  di.seases  of  the  myocardium  or  muscular  wall  of  the 
heart,  as  distinct  from  the  pericardium  and  endocardium, 
include  a  variety  of  different  conditions.  Those  which  are 
of  practical  and  clinical  importance,  and  which  we  shall 
therefore,  consider  in  detail,  are  : — 

1.  The  inflammatory  affections  and  their  results  (acute 
and  chronic  myocarditis,  fibroid  degeneration,  chronic  aneur- 
ismal  dilatation  of  the  cardiac  cavities). 

2.  Hypertrophy,  dilatation,  and  atrophy  of  the  heart. 

3.  The  various  forms  of  muscular  degeneration,  amongst 
which  the  fatty  form  is  of  the  most  importance  from  a  practical 
and  clinical  point  of  view. 

The  new  growths  of  the  heart,  which  form  a  fourth  group, 
are  extremely  rare,  and  are  of  more  interest  to  the  pathologist 
than  the  practical  physician. 

ACUTE   MYOCARDITIS. 

Definition. — Acute  inflammation  of  the  muscular  wall  of 
the  heart. 

There  is  considerable  difference  of  opinion  as  to  what 
should  and  what  should  not  be  included  under  the  head  of 
acute  myocarditis.  Some  authorities  consider  that  the  changes 
which  are  met  with  in  the  muscular  fibres  of  the  heart  in 
certain  febrile  affections,  notably  in  typhus  and  typhoid,  are 
inflammatory ;  and  Virchow  indeed  divides  cases  of  myo- 
carditis  into    two   groups,  viz.,  the  parenchymatous  and    the 


Aitiology  of  Acute  Myocarditis.  561 

interstitial ;  other  observers  doubt  the  occurrence  of  a  purely 
parenchymatous  inflammation  of  the  cardiac  wall,  and  think, 
that  in  all  cases  of  myocarditis,  alterations  are  to  be  detected 
in  the  fibrous  septa  and  blood  vessels,  which  lie  between  the 
muscular  fibres,  as  well  as  in  the  muscular  tissue  itself.  Per- 
sonally I  agree  with  the  latter  view,  and  I  am,  with  Gowers,^ 
in  the  habit  of  including  cases  of  so  called  parenchymatous 
myocarditis  under  the  head  of  degenerative  rather  than 
inflammatory  changes.  I  do  not,  of  course,  mean  to  imply 
that  myocarditis  is  never  observed  in  typhoid  and  typhus, 
but  only  that  the  ordinary  changes  (cloudy  swelling  and 
acute  fatty  changes)  which  occur  in  these  affections,  and 
indeed  in  all  cases  of  continued  pyrexia,  are  not  in  my 
opinion  of  an  inflammatory  nature. 

j^tiology. — Acute  myocarditis  is  very  rarely  primar}',  but 
usually  arises  in  the  course  of  some  general  affection.  Acute 
articular  rheumatism  is  the  disease /(^r  excellence  with  w^hich  it 
is  most  frequently  associated  ;  in  the  majority  of  these  cases 
{i.e.  of  rheumatic  myocarditis)  the  inflammatory  process  seems 
to  arise  in  the  pericardium  or  in  the  endocardium,  and  to 
extend  subsequently  to  the  muscular  substance  of  the  heart. 
In  some  rheumatic  cases  the  inflammation  is  probably  limited 
to  the  myocardium.  Inflammation  of  the  myocardium  is 
occasionally  met  with  in  pyaemia  and  puerperal  fever,  and 
in  cases  of  this  description  secondary  abscesses  may  form 
in  the  wall  of  the  heart.  New  growths,  which  are  of  rare 
occurrence  in  the  heart,  may  produce  inflammation  of  the 
muscular  tissue  which  surrounds  them.  Traumatic  injuries 
seem  occasionally  to  be  the  cause  of  acute  myocarditis.  Em- 
bolic plugging  of  branches  of  the  coronary  artery  also  seems 
in  some  cases  to  be  followed  by  changes  of  an  inflammatory 
character  in  the  cardiac  wall. 

Pathology. — In  some  cases,  the  inflammation  is  general  or 
involves  extensive  portions  of  the  wall  of  the  heart ;  in  others, 
it  is  local  or  limited  in  distribution.     The  ventricles  are  more 

'  Russell  Reynolds'  System  of  Medicine,  vol.  iv.  p,  529. 

N    N 


562  Diseases  of  the  Heart. 

frequently  affected  than  the  auricles.  After  birth  the  left 
ventricle  is  much  more  liable  to  be  affected  than  the  right  : 
during  intra-utcrinc  life  the  contrary  holds  good.  The  apex 
of  the  left  ventricle  seems  to  be  the  part  which  is  especially 
liable  to  be  attacked,  then  the  septum  ventriculorum,  then  the 
posterior  wall  of  the  organ. 

On  naked  eye  examination,  the  affected  portion  of  the 
heart  is,  in  the  earlier  stages,  of  a  dark  purple  or  bright  red 
colour,  the  result  of  the  increased  quantity  of  blood  which  it 
contains  ;  in  the  later  stages  it  may  be  paler  than  in  health. 
The  consistency  of  the  muscular  tissue,  more  especially  in  the 
later  stages  of  the  affection,  is  softer  than  normal.  According 
to  some  authorities  (Stein  quoted  by  Schroetter^)  the  myo- 
cardium is  sometimes  studded  throughout  with  spots  of  albu- 
menous  exudation,  which  have  a  glistening  appearance,  and 
resemble  little  deposits  of  fat  scattered  through  the  muscular 
tissue  ;  personally  I  have  not,  so  far  as  I  can  remember, 
observed  this  change. 

On  microscopical  examination,  the  vessels  of  the  myo- 
cardium are  seen  to  be  dilated  and  engorged ;  the  fibrous  septa 
between  the  muscular  fibres  and  around  the  blood  vessels  are 
more  or  less  infiltrated  with  cellular  elements  (leucocytes, 
red  blood  corpuscles,  and  proliferating  nuclei  of  the  cellular 
tissue,  see  figs.  233  and  234-),  and  in  some  rare  cases  (purulent 
myocarditis)  well  marked  collections  of  pus — small  abscesses 
— may  be  detected  under  the  pericardium  or  in  the  substance 
of  the  wall  of  the  heart.  The  muscular  elements  may  be 
little  altered,  but  in  typical  examples  of  acute  myocarditis 
they  are  swollen,  and  their  normal  striation  is  indistinct  or 
completely  absent  in  consequence  of  cloudy  swelling,  glassy 

'  ZicmssoCs  Cylclopicdia,  vol.  vi.  p.  228. 

^  In  the  preparation  from  which  figures  233  and  234  was  drawn,  the  fibrous 
septa  were  infiltrated  with  exudation  products  and  large  collections  of  leuco- 
cytes were  present  here  and  there  in  the  deeper  layer  of  the  pericardium.  The 
muscular  fibres  were  for  the  most  part  quite  healthy.  The  section  was  made  from 
an  advanced  case  of  valvular  disease.  In  typical  cases  of  acute  myocarditis,  the 
same  changes  which  are  present  in  the  perimysium  in  this  case  can  also  be 
observed,  but  in  addition  the  muscular  fibres  themselves  are  (?)  always  more  or 
less  affected  in  the  manner  described  in  the  text. 


■i  .....r^.^rt''^''"!}-^ 


A 


m 


Fig.  233. 


Fig.  231. — Mtiscvlar  fibres  in  sub-acute  myocarditis^  showing  great  enlcrgemerit  of  their  nuclei  {x  300). 

Fig.  231'. — Muscular  fibres  in  chronic  myocarditis  (x  250). 

a,  a,  muscular  fibres  transversely  divided,  showing  vacuoles ;  b,  b,  tLe   same   in  longitudiual 
fiection  ;  c,  c,  nuclei  within  the  vacuolated  fibres. 

Fig.  232. — Muscular  fibres  m  c/irordc  myocarditis  (x  250) 

The  fibres  aro  swollen  ;  their  transverse  strise  have  almost  comi^letely  disappeared ;  the  fibres 
are  granular,  but  not  fatty. 

Fig.  233. — Section  through  the  tcall  of  the  left  ventricle  in  a  case  of  chronic  mitred  disease  (^xabout  200). 

The  fibrous  tissue  between  the  muscular  fibres  is  increased,  and  infiltrated  with  leucocytes  and" 
red  blood  corpuscles  ;  the  muscular  fibres  are  healthy.,  wi,  m,  muscular  fibres;  f,  f,  fibrous  tissue; 
c,  connective  tissue  corpuscles;  /,/,  leucocytes ;  r,  r,  red  blood-corpuscles;  w,  blood-vessel. 

OIL'.DN.TfeTLlTHOO.  M=  U.«lCoH«(«C,|jT«C?  f 


•".*».*, 


^''"vSrt"  w2  SS/'f  «f f "'"''^  /'enc^rrft^,^  a.c/  acf>ce«<  part  of  the  muscnlar  wall  of  the 

formin?^tilksTot-^'H±?''V^'P''V=f'^^^'"'  *'  ^^^°"«  thickening  of  the  pericardium 
conUiW  fTt  cellsr  hl3  wLh  ''"T  ""Z  |«'^«°''Ttes;  t/,  the  deeper  laylr  of  the  pericardium, 
Wr^tef  S^e^^^fimulcSarfiw"'^  ^^^'  ^' «' ~1-  ^^-^  trauiversely  dfvided;  h^ 


Pathology  of  Acute  Myocarditis.  563 

degeneration,  or  fatty  changes  ;  the  affected  fibres  are  more 
brittle  than  usual,  and  tend  to  split  up  transversely  into  short 
fragments.  In  some  cases,  more  especially  in  purulent  myo- 
carditis, the  muscular  fibres  at  the  seat  of  the  inflammation 
may  be  entirely  destroyed,  and  a  mass  of  broken  down  tissue, 
consisting  of  granular  debris,  fatty  particles,  leucocytes,  and  a 
few  red  blood  corpuscles,  may  be  all  that  remains.  In  sub- 
acute myocarditis,  the  nuclei  of  the  muscular  fibres  are  often 
enormxously  enlarged.     (See  figs.  231  and  237.) 

Pathological  physiology. — The  effects  produced  by  myo- 
carditis vary  very  considerably  in  different  cases,  and  depend 
upon  the  severity,  extent,  and  character  of  the  inflammation. 
When  extensive  portions  of  the  muscular  wall  of  the  heart  arc 
implicated,  the  force  of  the  cardiac  pump  is  seriously  impaired, 
and  acute  dilatation  of  the  affected  cavities  may  result ;  regur- 
gitation due  to  '  muscular'  and  '  relative'  incompetence  of  the 
mitral  or  tricuspid  orifices  also  occurs  in  cases  of  this  descrip- 
tion. Auriculo-ventricular  regurgitation  may  also  result  from 
a  local  inflammation  of  the  muscular  fibres  surrounding  the 
mitral  or  tricuspid  orifices,  the  other  parts  of  the  cardiac  wall 
being  healthy.  Acute  cardiac  aneurisms,  i.e.  acute  local  bulg- 
ings  of  some  part  of  the  cardiac  wall,  and  rupture  of  the  heart 
are  occasionally  met  with  as  the  result  of  inflammation  and 
softening,  limited  to  some  particular  part  of  the  wall  of 
the  organ.  When  an  abscess  forms  it  may  make  its  way 
cither  externally  into  the  pericardium,  producing  acute 
purulent  pericarditis,  or  internally  through  the  endocardium  ; 
in  the  latter  case,  which  is  probably  of  very  rare  occurrence, 
the  contents  of  the  abscess  escape  into  the  circulation,  and 
may  add  to  the  septic  (pyaemic)  symptoms,  which  are  usually 
present  in  cases  of  this  description.  (Purulent  myocarditis 
is  rarely  met  with  except  in  cases  of  pyaemia.)  When  the 
abscess  occupies  the  septum  ventriculorum,  perforation  of  the 
septum  may  be  produced,  and  a  communication  established 
between  the  two  ventricular  cavities.  Communication  be- 
tween the  two  auricles  might  be  produced  in  a  similar  manner, 
i.e.  by  the  bursting  of  an  abscess,  the  result  of  ulcerative  endo- 
carditis in  the  auricular  septum. 


564  Diseases  of  tJie  Heart. 

Symptoms  and  physical  signs. — The  s)'mptoms  and  ph}-sical 
signs  of  acute  myocarditis  are  for  the  most  part  very  inde- 
finite. In  the  shghter  forms  of  the  disease,  such  as  are,  I 
believe,  of  much  more  frequent  occurrence  in  acute  rheumatism 
than  is  generally  supposed,  symptoms  and  signs  indicative  of 
myocarditis  may  be  entirely  absent  or  extremely  slight.  In 
more  severe  cases,  the  patient  usually  complains  of  some 
uneasiness,  and  occasionally  of  actual  pain  in  the  region  of 
the  heart ;  a  feeling  of  tightness,  shortness  of  breath,  and  pal- 
pitation are  frequently  experienced.  There  is,  too,  more  or 
less  (often  extreme)  exhaustion,  langour,  and  debility,  and 
frequent!}'  a  short  dry  cough.  In  severe  cases,  the  signs  of 
venous  engorgement  and  stasis,  such  as  have  been  described 
under  the  head  of  acute  endocarditis  and  chronic  valvular 
lesions,  are  present.  The  pulse  is  considerably  quicker  than 
normal  ;  in  the  earlier  stages  of  the  disease  it  may  be  unusu- 
ally irritable  ;  in  the  latter  stages  it  is  small,  and  often  ver}' 
irregular.  There  is  generally  some  pyrexia  ;  the  increased 
temperature  partly  depending  upon  the  myocarditis,  but 
being  for  the  most  part  due  to  the  primaiy  affection  with 
which  the  myocarditis  is  associated, — acute  rheumatism  for 
example — or  to  associated  pericarditis  or  endocarditis.  In 
cases  of  purulent  myocarditis,  a  suppurative  temperature,  cha- 
racterised by  frequent  ups  and  downs,  and  associated  with 
rigors  and  sweatings,  is  usually  observed. 

On  examining  the  heart,  the  physical  signs  of  pericarditis, 
or  of  endocarditis,  which  are  so  generally  associated  with  acute 
myocarditis  can  usually  be  detected.  In  uncomplicated  cases, 
i.e.  where  there  is  no  associated  pericarditis  or  endocarditis, 
the  action  of  the  heart  may,  in  the  earlier  stages,  be  unusually 
irritable.  Soon,  however,  fhe  signs  of  cardiac  failure,  dilata- 
tion and  auriculo-ventricular  regurgitation  become  apparent. 
The  impulse  becomes  weak  or  altogether  imperceptible ;  the 
area  of  dulness  more  or  less  increased  ;  the  first  sound  short 
and  faint,  or  replaced  in  the  mitral  and  tricuspid  area.s,  by  a 
a  soft  blowing  murmur. 

Diagnosis. — The  diagnosis   is   in    many   cases   difficult   or 


Diagnosis  of  Acute  Myocarditis.  565 

impossible.  Acute  myocarditis  may  be  suspected,  when  in 
addition  to  more  or  less  pyrexia,  the  symptoms  and  signs  of 
cardiac  failure  (perhaps  preceded  b}'^  indications  of  cardiac  irri- 
tability) are  acutely  developed,  in  the  course  of  a  disease,  such 
as  acute  rheumatism,  in  which  inflammation  of  the  myocardium 
is  apt  to  occur.  A  positive  diagnosis  of  acute  myocarditis  can 
only  be  given,  when,  in  addition,  the  observer  feels  satisfied 
that  the  symptoms  and  signs  do  not  depend  upon  pericarditis 
and  endocarditis.  (Pericarditis  and  endocarditis  are  frequently 
complicated,  as  we  have  already  seen,  with  inflammation  of 
the  muscular  layer  of  the  heart ;  and  in  cases  of  acute  peri- 
carditis and  acute  endocarditis  it  is  often  extremely  difficult 
to  determine  what  proportion  of  the  symptoms,  so  to  speak, 
depends  upon  the  inflammation  of  the  pericardium,  of  the 
endocardium,  and  of  the  myocardium  respectively.) 

The  differential  dim^nosis  of  acute  endocarditis  and  acute 
myocarditis  is  especially  difficult,  and  in  many  cases  impos- 
sible. It  may  be  impossible,  for  example,  in  a  case  of  rheu- 
matic fever,  in  which  mitral  regurgitation  is  developed  at  an 
early  stage  of  the  case,  to  say  w^iether  the  incompetence  is 
'  muscular'  and  due  to  myocarditis,  or  whether  it  depends 
upon  endocarditis.  But  into  the  details  of  this  question, 
which  have  been  discussed  in  treating  of  acute  endocarditis 
(see  p.  373)  I  need  not  again  enter. 

The  presence  of  purulent  myocarditis  may  be  suspected, 
when  the  symptoms  and  signs  of  cardiac  weakness  and  irrita- 
bility are  acutely  developed  in  the  course  of  pyaemia  or  other 
conditions,  in  which  purulent  myocarditis  is  apt  to  arise.  If 
in  addition  acute  pericarditis  is  very  quickly  developed,  or,  if 
symptoms  of  arterial  pyaemia  rapidly  arise,  the  obsei-ver  may 
suspect  that  an  abscess  in  the  myocardium  has  ruptured  into 
the  pericardium  or  into  the  interior  of  the  heart.  It  is 
seldom  possible  to  do  more  in  the  way  of  diagnosis  than 
suspect  these  conditions  ;  there  are  many  fallacies  which  deter 
a  careful  and  thoughtful  investigator  from  committing  himself 
to  a  positive  opinion  in  cases  of  this  description,  though  the 
imperfectly  informed,  and  often  plausible  physician  who  has 
no  difficulty  in  giving  a  sharply  defined  diagnosis  in  any  and 


566  Diseases  of  the  Heart. 

every  case  (and  who,  it  may  be  observed  is,  often  unable  to 
g^ive  the  grounds  for  his  opinion,  or  to  appreciate  correctly 
the  arguments  which  may  be  brought  against  it)  may  occa- 
sionally make  a  happy  hit. 

Prognosis. — Acute  myocarditis,  in  its  more  severe  and 
pronounced  forms,  is  a  very  serious  affection,  and  adds,  as  we 
have  previously  seen,  very  materially  to  the  danger  of  any 
other  cardiac  affection.  Slight  degrees  are,  I  think,  of  much 
more  frequent  occurrence  in  acute  rheumatism  than  is  gener- 
ally supposed,  and  are,  I  believe,  frequently  recovered  from. 
In  attempting  to  gauge  the  gravity  of  each  individual  case, 
the  amount  of  cardiac  weakness  (which  is  determined  by  ob- 
serving the  force  of  the  cardiac  impulse  ;  the  extent  of  the 
cardiac  dilatation;  the  character  of  the  first  sound;  the 
severity  of  the  symptoms  indicative  of  mechanical  derange- 
ment of  the  venous  circulation  ;  and  especially  the  condition 
of  the  radial  pulse),  is  the  point  which  must  be  chiefly  relied 
upon.  It  must,  however,  be  remembered  in  considering  the 
prognosis,  that  a  localised  inflammation  of  the  cardiac  muscle, 
insufficient  to  produce  any  very  distinct  or  marked  symptoms 
and  signs,  may  produce  such  an  amount  of  softening  of  the 
cardiac  wall  as  may  result  in  the  formation  of  an  acute  aneurism 
or  may  cause  rupture  of  the  organ.  Localised  myocarditis 
leading  to  such  complete  softening  as  is  likely  to  produce 
acute  aneurism  or  rupture  of  the  heart,  is  seldom  seen  in  rheu- 
matic cases.  It  is  more  likely  to  be  produced  in  the  purulent 
myocarditis,  or  as  the  result  of  the  embolic  plugging  of  the 
coronary  artery  or  its  branches.  Purulent  myocarditis  is 
almost  certainly  fatal. 

TrcatJHoit. — The  same  general  measures  which  have  been 
recommended  in  the  treatment  of  acute  pericarditis  and  acute 
endocarditis,^  must  be  adopted,  the  greatest  care  being  taken 
to  avoid  everything  which  is  likely  either  to  excite  or  depress 
the  action  of  the  heart.      The  main  object  of  treatment  (for 

'  The  reader  is  recommended  tc  refer  to  the  treatment  of  acute  pericarditis 
and  acute  endocarditis  (see  pp.  336  and  337). 


Treatment  of  Actitc  Myocarditis.  567 

we  know  of  no  means  of  cutting  short  and  arresting  the 
cardiac  inflammation)  is  to  sustain  the  strength  of  the  heart, 
and  at  the  same  time  to  reheve  the  organ  from  all  strain,  and  to 
keep  it  as  tranquil  as  possible. 

In  rheumatic  cases,  salicylate  of  soda,  which  exerts  a 
decidedly  depressing  effect  upon  the  organ,  must,  as  soon  as 
there  is  reason  to  suspect  the  onset  of  acute  myocarditis,  be 
at  once  discontinued,  though,  according  to  Dr  Maclagan,  salicin 
itself  may  still  be  given.  Although  I  am  quite  satisfied  that 
salicylate  of  soda  is  more  depressing  than  salicin,  I  prefer  to 
err  on  the  side  of  caution.  In  cases,  then,  of  acute  rheuma- 
tism, in  which  there  is  distinct  evidence  of  myocarditis,  I 
would  recommend  that  not  only  salicylate  of  soda,  but  also 
that  salicin  be  discontinued,  and  that  quinine,  or  quinine  and 
bicarbonate  of  potash,  be  substituted  for  these  drugs.  The 
patient  must  be  kept  at  perfect  rest  in  bed,  and  all  sources  of 
agitation  or  excitement  rigidly  avoided.  During  the  stage  of 
cardiac  excitement  and  irritability,  which  is  often  observed  at 
the  commencement  of  the  attack,  belladona  and  digitalis  are 
the  most  useful  drugs.  During  the  subsequent  stages  of  the 
disease,  small  doses  of  digitalis  and  quinine  may  be  given. 
In  the  treatment  of  acute  myocarditis,  it  is  very  important  to 
look  out  for  symptoms  and  signs  of  cardiac  failure,  and  when 
necessary  to  strengthen  and  stimulate  the  action  of  the  heart. 
One  of  the  greatest  dangers  is  failure  of  the  heart's  action, 
and  it  is  absolutely  necessary  in  all  cases  in  which  indications 
of  cardiac  failure  arise  (notwithstanding  the  risk  of  producing 
rupture  in  those  cases  in  which  advanced  localised  softenings 
are  present)  to  administer  freely,  alcoholic  and  ammoniacal 
stimulants,  ether,  and  digitalis.  Other  symptoms  and  com- 
plications, such  as  pain  over  the  praecordia,  shortness  of  breath, 
cough,  dropsy,  embolic  infarctions,  etc.,  must  be  treated  by 
appropriate  remedies.  In  septic  cases,  and  in  cases  of  sus- 
pected purulent  myocarditis,  the  measures  which  have  been 
recommended  for  the  treatment  of  acute  ulcerative  endocarditis 
may  be  employed. 


568  Diseases  of  the  Heart. 

CHRONIC   MYOCARDITIS. 
Synonym. — Fibroid  degeneration  of  the  heart. 

Definition. — Chronic  inflammation  of  the  muscular  wall  of 
the  heart.  In  this  condition,  which  for  practical  purposes 
may  be  considered  synonymous  with  fibroid  degeneration  of 
the  heart,  bands  of  fibrous  tissue  are  developed  in  the  wall  of 
the  heart  and  around  the  muscular  fibres,  which  become  atro- 
phied, as  will  be  presently  described. 

yEtio/ogy  and  Pathology. — Chronic  myocarditis  or  fibroid 
degeneration  of  the  heart,  is,  in  many  cases,  the  direct  result  of 
a  previous  attack  of  acute  rheumatic  myocarditis.  In  cases  of 
this  description,  the  pericardium  and  endocardium  are  usually 
at  the  same  time  implicated,  and  chronic  thickening  of  one 
or  other,  or  both,  of  these  structures  is  found  after  death. 
It  is  generally  supposed  that  the  myocarditis,  which  is  the 
starting  point  of  the  fibroid  change,  is  secondary  to  an 
mflammation  of  the  pericardium  or  endocardium.  Possibly  in 
some  cases,  as  Dr  Hilton  Fagge  supposed,  the  order  of  events 
is  reversed,  and  the  thickening  of  the  pericardium  and  endo- 
cardium is  the  result  of  a  fibroid  change  commencing  in  the 
myocardium.  In  other  cases  of  rheumatic  origin  (but  these 
are  much  more  rare),  the  myocardium  is  alone  affected,  the 
pericardium  and  endocardium  being  healthy.  It  is  interesting 
to  obser\'e  that  in  most  cases  of  fibroid  degeneration,  even 
where  the  whole  thickness  of  the  heart  wall  is  involved,  a 
narrow  band  of  muscular  fibres  usually  remains  just  internal 
to  the  endocardium.  This  appearance  is  well  seen  in  figs.  176, 
T)2,'^,  and  245.  In  the  preparation,  represented  in  fig.  176,  the 
endocardium  and  pericardium  are  enormously  thickened  ;  in 
that  case,  in  which  endocarditis,  pericarditis,  and  myocarditis 
were  present,  the  condition  was  of  rheumatic  origin.  In  the 
preparation  shown  in  fig.  245,  the  pericardium  and  endo- 
cardium are  healthy  ;  in  the  latter  case  the  condition  was 
probably  of  syphilitic  origin. 

In  some  cases,  the  fibroid  change  is  slowly  and  gradually 
developed,  and  is  chronic  from  the  first.     Some  of  these  cases 


Fig.  235. — Fibroid  degeneration  of  the  heart,  sliowing  atrophy  of  one  of  the  papillary  muscles. 

(^iSutural  size.) 

A  piece  of  whalebone  has  been  placed  beneath  the  atrophied  papillary  muscle ;  its  chordae 
tendinese  are  somewhat  thickened  and  retracted.  The  letter  a,  points  to  the  opposite  papillary 
which  is  healthy. 


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Fig.  237 — Section  throvgh  the  endocardium  and  adjacent  part  of  the  wall  of  the  left  ventricle  in  endo- 
myocarditis.     {Magnifien  about  300  diameters.') 

a,  thickened  endocardium  confaining  numerous  corpuscles  and  spindle  cells,  b,  a  band  of  muscular 
fibres  which  still  remains  adjacent  to  the  endocardium ;  some  of  the  muscular  fibres  contain  large 
nuclei  (c,  c).  An  extensive  tract  of  fibroid  tissue  (the  endocardial  end,  rf,  can  only  be  seen  iu  the 
figure),  is  situated  in  the  wall  of  the  left  ventricle;  it  contains  numerous  corpuscles  and  nuclei. 
f,  e,  veins  surrounded  by  fibroid  tissue.  ./;  /,  arteries,  the  walls  of  which  are  very  thick.  (The 
coronary  arteries  were  very  atheromatous;  iii  one  part  of  the  section  from  which  this  drawing  was 
made,  a  haemorrhage,  probably  due  to  rupture  of  a  branch  of  the  coronary  artery,  was  seen.) 


Fig.  238. — Section  thrvugh  the  wall  of  the  left  ventricle  in  chronic  myocarditis, showing  uiu/unms 
blood-vessch  and  the  remains  oj' muscular  Jthris  in  the  midst  of  the  fibrous  tissue.  (^Magnified 
about  2d0  diamettrs.) 

a,   fibrous   tissue ;    b,  blood-vessel ;  c,   c,   atropLied   muscular  fibres ;    d,  leucocyte,   and 
e,  nucleus  of  fibrous  tissue. 


Fig.  239. — Another  portion  of  the  same  preparation  showing  healthy  and  atrophied  muscular  fibres 
in  the  midst  of  fibrous  tissue.     (^Magnified  about  300  diameters.') 


Fig.  240. — Section  throwjh  the  wall  of  the  left  ventricle  in  chronic  myocarditis.    (^Magnifed  about 

50  diameters.') 

a,  a,  muscular  fibres  transversely  divided ;  i,  6,  empty  spaces  from  which  the  muscular  fibres 
have  fallen  out ;  c,  c,  fibrous  tissue  between  the  muscular  fibres ;  v,  large,  and  v',  small  blood-vessels 
transversely  diNnded. 


Fig.  241.— Section  through  the  wall  of  the  left  ventricle  in  chronic  myocarditis.     (Magnifed  about 

250  diameters.) 

a,  a,  healthy  muscular  fibres  transversely  divided ;  b,  b,  vacuolated  muscular  fibres,  some  of 
theincontaiuing  nuclei,  c;  d,  d,  d,  empty  spaces  from  which  the  muscular  fibres  have  fallen  out; 
e,e,  fibrous  tissue  ;  /,./;  the  remains  of  atropLiexi  muKcular  fibres  (some  of  which  are  mere  collections 
of  pigment);  v.v,  blood-vessels;  g,g,  the  walls  of  large  spaces  (containing  blood)  situated  in  the 
midst  of  the  fibrous  tissue.    The  letters  A,  A,  A,  are  placed  in  these  spaces. 

B.  «.'«  ..rr  .T  L,T«o..  Sfi^,iU....C  b..r'  £«■" 


Etiology  and  Pathology  of  Acute  Myocarditis.   569 

seem  also  to  be  of  rheumatic  origin  ;  others  are  undoubtedly- 
due  to  syphilis.  Long  continued  alcoholic  excess  is  probably 
another  cause  of  the  condition.  In  a  considerable  proportion 
of  cases  of  granular  kidney,  the  hypertrophied  heart  (which 
is  developed  in  that  condition  unless  the  organ  is  so  damaged 
by  previous  disease  as  to  be  incapable  of  becoming  hyper- 
trophied) presents,  on  microscopical  examination,  well-marked 
fibroid  changes.  Probably  in  some  cases  of  this  description, 
the  cirrhosis  of  the  kidney  and  the  cirrhosis  or  fibroid  degene- 
ration of  the  heart  are  both  due  to  chronic  alcoholism.  The 
heart,  represented  in  fig.  235,  from  which  the  section  shown 
in  fig.  240  was  made,  was  a  typical  example  of  fibroid  degenera- 
tion, the  papillary  muscles  in  particular  being  extremely  atro- 
phied. The  patient  was  an  old  woman  who  for  years  had 
indulged  freely  in  whisky,  and  who  had  never,  so  far  as 
I  could  ascertain,  suffered  from  rheumatism.  The  kidneys 
were  typically  cirrhotic,  and  yet  the  heart  was  not  hyper- 
trophied. Possibly  in  this  case  the  fibroid  degeneration  of 
the  heart  was  the  first  event,  the  kidney  lesion  followed,  and 
owing  to  the  damaged  condition  of  the  cardiac  muscle,  hyper- 
trophy of  the  left  ventricle  could  not  occur.  The  fibroid  lesion 
of  the  cardiac  wall  was  very  probably  in  this  case  (in  some 
measure  at  all  events)  the  result  of  alcohol. 

Long  continued  venous  engorgement  of  the  wall  of  the 
heart,  such  as  results  from  mitral  disease,  may  also  lead  to 
the  production  of  fibroid  changes  between  the  muscular  fibres, 
just  as  it  may  lead  to  a  form  of  cirrhosis  of  the  liver  or  of  the 
kidney  ;  indeed,  as  has  been  pointed  out  by  Dr  Charlewood 
Turner,  the  perimysium,  or  fibroid  tissue  around  the  muscular 
fibres  of  the  heart,  is  increased  in  many  cases  of  hypertrophy 
resulting  from  valvular  disease.  Dr  Turner  thinks  that  the 
perimysium  is  thickened  in  the  great  majority  of  cases  of 
hypertrophy  of  the  heart  whether  the  hypertrophy  result  from 
chronic  Bright's  disease  or  from  valvular  lesions.  I,  too,  have 
found  changes  similar  to  those  which  he  has  described  in  a 
considerable  number  of  cases,  but  my  observations  do  not  as 
yet  warrant  me  in  believing  that  this  fibroid  change  in  the  myo- 
cardium is  so  frequently  present  as  Dr  Turner  seems  to  suppose. 


5/0  Diseases  of  the  Heart. 

Traumatic  injuries  in  some  cases  seem  to  have  been  the 
exciting  cause  of  the  condition.  In  pseudo-hypertrophic  para- 
l\'sis,  fibroid  patches  are  sometimes  seen  in  the  wall  of  the 
heart,  and  undoubtedly  owe  their  origin  to  the  causes  which 
produced  the  fibroid  and  atrophic  changes  in  the  voluntary 
muscle. 

Males  are  probably  more  frequently  affected  with  fibroid 
degeneration  of  the  heart  than  females.  The  condition  is 
seldom  met  with  in  young  subjects,  except  as  the  result  of 
rheumatic  causes  or  pseudo-hypertrophic  paralysis ;  it  is 
much  more  common  after  than  before  thirty  years  of  age. 

In  some  cases  the  fibroid  change  is  uniformly  distributed 
through  large  portions,  or  through  the  whole,  of  the  organ  ; 
and  in  cases  of  this  description,  it  probably  owes  its  origin  to 
long  continued  venous  engorgement  or  chronic  alcoholism. 
In  others,  the  fibroid  change  is  much  more  marked  in,  or  is 
confined  to,  limited  portions  of  the  wall  of  the  heart.  In  intra- 
uterine life  the  right  ventricle  is  the  part  which  is  said  to  be 
chiefly  affected.  After  birth  the  left  ventricle  and  the  sep- 
tum ventriculorum  are  the  parts  which  are  chiefly  attacked, 
but  my  experience  does  not  altogether  agree  with  those  who 
believe  that  the  fibroid  change  is  usually  confined  to  the  cavity 
of  the  left  ventricle.  I  admit,  however,  that  the  lesion  is,  as 
a  rule,  more  extensive  and  more  advanced  in  that  cavity  than 
in  the  other  parts  of  the  organ. 

The  naked  eye  appearances  differ  in  accordance  with  the 
stage  of  the  lesion  and  the  distribution  of  the  fibroid  tissue. 
When  the  whole  thickness  of  the  heart  is  involved,  and  the 
fibroid  change  consists  in  a  thickening  of  the  perimysium  around 
individual  fibres  (such  as  is  shown  in  fig.  240)  rather  than  the 
production  of  large  masses  of  fibroid  tissue,  there  is  little  or 
no  alteration  visible  to  the  naked  eye  ;  the  heart  perhaps  looks 
hypertrophied  ;  its  colour  is  perhaps  paler  than  normal,  and 
its  consistency  somewhat  firmer  than  natural.  When,  on  the 
contrary,  the  fibroid  change  is  more  localised  and  large  masses 
of  new  tissue  are  formed  between  and  around  the  muscular 
fibres  (see  figs.  176  and  236),  the  naked  eye  changes  may  be 
very  visible  ;  the  masses  of  fibroid  tissue  being  of  a  yellow  or 


Pathology  of  CJiroiiic  Myocarditis.  571 

yellowish  white  colour  stand  out  prominently,  usually  in  the 
form  of  streaks  or  bands  between  the  red  or  reddish-brown 
masses  of  muscle.  The  wall  of  the  heart  at  the  affected  part 
is  tougher  than  normal,  in  some  cases  it  is  almost  cartilaginous 
in  hardness,  in  others  it  cuts  '  gritty,'  owing  to  the  deposit  of 
calcareous  particles  in  the  midst  of  the  fibroid  tissue. 

It  not  unfrequently  happens  that  the  adjacent  parts  of  the 
pericardium  or  endocardium  are  considerably  thickened,  and 
the  thickness  of  the  cardiac  wall,  taken  as  a  whole,  is  increased. 
(See  fig.  236.)  In  other  cases,  the  wall  of  the  heart  at  the  seat 
of  the  lesion  is  thinner  than  usual ;  and  should  it  be,  as  it 
often  is,  at  the  same  time  dilated,  a  local  bulging  or  aneurismal 
dilatation  may  be  formed  at  the  affected  spot.  (See  fig.  245.) 
The  papillary  muscles  are  the  parts  which  are  most  frequently 
affected  by  fibroid  degeneration ;  they  look  shrunken,  flattened, 
and  atrophied;  they  loose  their  normal  reddish  colour,  and 
become  pale  and  white ;  the  chordae  tendinea;  may  be  thickened 
and  retracted. 

On  microscopical  examination,  masses  of  fibroid  tissue 
which  stain  of  a  bright  pink  colour  with  picro-carmine,  are 
seen  between  and  around  the  muscular  fibres.  In  those  cases 
in  which  the  fibroid  change  is  diffused  throughout  the  heart, 
the  individual  muscular  fibre  may  be  surrounded  with  a 
band  of  fibrous  tissue  (see  fig.  240),  which  in  recent  cases  (in 
sub-acute  myocarditis)  is  rich  in  nuclei  and  spindle-celled  ele- 
ments. (See  fig.  237.)  In  other  cases,  and  more  particularly 
in  those  cases  in  w^hich  the  fibroid  change  is  localised  in  one 
particular  part  of  the  heart,  large  masses  of  fibroid  tissue  are 
placed  between  masses  of  muscular  tissue.  (See  figs.  176  and 
236.)  In  cases  of  this  description,  the  fibroid  patches  consist, 
for  the  most  part,  of  wavy  bundles  of  white  fibrous  tissue 
which  stain  pink  with  picro-carmine.  In  other  and  rarer  cases, 
— and  these,  so  far  as  my  experience  goes,  seem  to  be  chiefly 
syphilitic, — the  new  growth  contains  large  quantities  of  ex- 
tremely fine  elastic  fibres  which  stain  yellow  with  picro-carmine. 

The  masses  of  fibroid  tissue  are  richly  supplied  with  blood ; 
indeed,  in  some  cases,  enormous  vessels  are  found  in  the  midst 
of  these  fibroid  growths.     The  muscular  fibres,  surrounded  by 


572  Diseases  of  the  Heart. 

and  adjacent  to  the  fibroid  growth,  undergo  a  gradual  process 
of  atrophy,  and  may  entirely  disappear,  their  former  position 
being  perhaps  indicated  by  small  masses  of  granular  yellow 
pigment.  In  this  process  of  atrophy,  as  Dr  Charlewood  Turner 
has  so  well  described,  and  as  many  of  my  preparations  beauti- 
fully demonstrate,  the  fibrill^e  disappear  from  the  central  parts 
of  the  fibres,  leaving  well  defined  spaces,  in  which  large  nuclei 
arc  sometimes  seen.     (See  c.  fig.  231'.) 

In  some  cases,  and,  so  far  as  my  experience  teaches,  in 
syphilitic  cases,  the  arteries  in  the  neighbourhood,  or  in  the 
midst  of  the  fibroid  patches,  may  be  narrowed  by  endarteritis 
obliterans.     (See  figs.  245  and  273.) 

In  pseudo-hypertrophic  paralysis,  judging  from  one  case 
which  I  have  been  able  to  examine  carefully,  the  fibroid 
tissue  seems,  in  part  at  least,  to  be  derived  from  the  muscular 
fibres  themselves.  In  the  acute  and  subacute  forms  of  myo- 
carditis, some  of  the  muscular  fibres  are  usually  found  in  a 
condition  of ■  fatty  degeneration.  In  the  more  chronic  forms, 
such  as  are  commonly  classed  under  the  head  of  fibroid  dege- 
neration, fatty  degeneration  of  the  muscular  elements  is  not 
generally  seen,  but  the  muscular  fibres  seem  to  disappear  by  a 
process  of  simple  atrophy  ;  ultimately  they  may  completely 
disappear,  their  place  being  represented  by  a  few  pigment 
granules.     (See  figs.  238,  239,  and  240.) 

Pathological  Physiology. — The  effect  of  chronic  myocarditis, 
or  fibroid  degeneration  of  the  heart,  as  we  may  term  it,  is  to 
produce  atrophy  of  the  proper  muscular  elements,  and  there- 
fore to  impair  the  force  of  the  cardiac  pump,  and  the  resist- 
ance which  the  cardiac  walls  naturally  opjDOse  to  the  blood 
pressure.  The  effects,  of  course,  vary  with  the  extent  of  the 
lesion,  and  the  cavity  or  cavities  which  happen  to  be  affected. 
When  the  fibroid  change  is  pretty  generally  diffused — 
through  the  wall  of  the  left  ventricle,  for  example — there 
is  a  tendency  to  general  dilatation  of  that  cavity  ;  the  driving 
power  of  the  left  ventricle  is  decreased,  less  blood  is  conse- 
quently expelled  into  the  arterial  system  than  under  normal 
circumstances,  and  blood  tends  to  stagnate  in  the  parts  of 
the  circulation    behind    the    affected   cavity,   i.e.    behind    the 


Symptoms  and  Signs  of  Chronic  Myocarditis.   573 

cavity  of  the  left  ventricle  ;  defective  muscular  closure,  i.e. 
'muscular'  incompetence,  at  the  mitral  orifice,  may  then  be 
established. 

When,  on  the  contrary,  the  fibroid  change  is  limited  to  one 
particular  part  of  the  heart,  say  to  the  wall  of  the  left  ventricle 
in  the  neighbourhood  of  the  apex,  as  in  fact  it  often  is,  the 
driving  power  of  the  left  ventricle  is  little  if  at  all  impaired, 
there  is  little  or  no  engorgement  of  the  circulation  behind,  no 
'  muscular '  incompetence  at  the  mitral  orifice  ;  the  resisting 
power  of  the  ventricular  wall  at  the  seat  of  the  lesion  is,  how- 
ever, weakened,  and  a  local  bulging  or  aneurismal  dilatation, 
which  in  some  cases  ruptures  and  causes  sudden  or  instan- 
taneous death,  may  be  produced. 

When  again  the  papillary  muscles  are  affected  and  atro- 
phied, the  perfect  working  of  the  mitral  valve  is  apt  to  be 
interfered  with,  and  mitral  incompetence  produced. 

In  some  cases,  the  fibroid  mass  instead  of  dilating  under 
the  pressure  of  the  blood  gradually  contracts,  just  as  an  ex- 
ternal cicatrix  (a  cicatrix  in  the  skin,  for  example)  does. 
Stenosis  of  the  conus  anteriosus  (true  stenosis  of  the  heart), 
a  condition  to  which  I  have  alluded  in  speaking  of  stenosis  of 
the  pulmonary  artery,  seems  to  be  due  to  the  contraction  of  a 
circular  band  of  fibrous  tissue — the  result  of  foetal  endocar- 
ditis— developed  all  round  the  wall  of  the  conus. 

Symptoms  and  pJiysical  signs. — The  symptoms  and  physi- 
cal signs  of  chronic  myocarditis  are  even  more  obscure  and 
indefinite  than  those  of  the  acute  form. 

The  diffuse  variety  is  characterised  by  the  usual  symptoms 
and  indications  of  failure  of  the  cardiac  pump,  viz.,  shortness 
of  breath,  in  some  cases  only  felt  on  exertion,  in  others  {i.e. 
in  advanced  cases)  constant  and  very  distressing  (extreme 
orthopnea)  ;  cough  ;  more  or  less  cyanosis  ;  subcutaneous 
oedema,  etc.  In  some  cases,  pain  in  the  region  of  the  heart  is 
complained  of,  and  in  one  case  at  least,  I  have  met  with 
well-marked  symptoms  of  angina  pectoris.  In  advanced 
cases,  the  radial  pulse  is  unusually  small  and  feeble,  often 
irregular    and    intermittent  ;    in  some   cases    it  is   of  normal 


5  74  Diseases  of  the  Heart. 

frequency  ;  in  others  slower ;  in  others  again  considerably 
quicker  than  natural. 

In  advanced  stages  of  the  disease,  the  impulse  of  the  heart 
is  weak  or  altogether  absent ;  the  praecordial  dulness  is  usually 
more  or  less  increased  ;  the  first  sound  short  and  feeble,  or 
replaced  by  mitral  or  tricuspid  systolic  murmurs. 

Limited  fibroid  patches  do  not,  as  a  rule,  give  rise  to  any 
symptoms  or  physical  signs,  but  to  these  cases  I  will  again 
more  particularly  refer  under  the  head  of  cardiac  aneurisms. 

Diagnosis. — The  diagnosis  of  fibroid  degeneration  of  the 
heart  is  always  somewhat  difficult  and  uncertain.  It  may  be 
suspected,  when  there  are  well-marked  symptoms  and  signs 
of  cardiac  weakness,  and  when  the  observer  is  able  to  satisfy 
himself  that  these  conditions  do  not  depend  upon  a  chronic 
valvular  lesion,  or  upon  fatty  degeneration  of  the  cardiac 
muscle.  In  short,  in  making  the  diagnosis  we  first  deter- 
mine by  the  help  of  the  symptoms  and  physical  signs  that 
the  heart  is  weak  {i.e.  chronically  weak) ;  and  secondly,  by  the 
method  of  exclusion,  we  satisfy  ourselves  that  the  cause  of 
that  weakness  is  fibroid  degeneration,  i.e.  we  conclude  from 
the  history,  general  condition  of  the  patient,  and  physical 
examination  of  the  heart,  that  there  is  no  other  cause  of 
chronic  cardiac  weakness  present.  But  to  this  point  I  will 
again  more  fully  refer  in  treating  of  the  differential  diagnosis 
of  fatty  heart. 

When  in  addition  there  is  reason  to  suppose  from  the 
history  of  the  case,  or  from  the  nature  of  the  physical  signs, 
that  the  pericardium  is  adherent,  the  diagnosis  of  fibroid 
degeneration  of  the  heart  wall  may  be  more  confidently  made. 

Prognosis. — Chronic  myocarditis  or  fibroid  degeneration 
seriously  impairs  the  functional  activity  of  the  part  of  the 
heart  which  is  afifected  by  it ;  and  since  the  fibroid  tissue 
cannot  be  removed  by  treatment,  the  prognosis  is  very  un- 
favourable. Sudden  death  not  unfrequently  occurs  in  cases  of 
chronic  myocarditis  ;  in  some  cases  of  this  description  there 
has  been  no  complaint  or  suspicion  of  cardiac  derangement 


Treatment  of  CJi7^onic  Myocai'ditis.  575 

during  life ;  in  some  cases,  the  fatal  result  it  is  due  to  sudden 
arrest  of  the  cardiac  contractions  and  syncope  ;  in  others, 
though  these  are  of  very  rare  occurrence,  to  the  rupture  of  a 
cardiac  aneurism. 

Treatment. — Since  it  is  impossible  to  remove  the  fibroid 
patches  and  to  restore  the  atrophied  muscular  fibres,  the 
treatment  is  necessarily  palliative.  The  main  indications  are 
to  avoid  all  cardiac  strain,  and  everything  likely  to  cause 
sudden  over-distention  of  the  organ.  The  patient's  life  should 
be  emphatically  a  quiet  one,  though  a  certain  amount  of  gentle 
out-door  exercise,  sufficient  to  maintain  the  general  health, 
but  insufficient  to  cause  shortness  of  breath,  or  any  feeling  of 
cardiac  distress,  or  to  produce  fatigue,  is  generally  beneficial. 
The  bowels  must  be  carefully  regulated,  and  all  straining  at 
stool  avoided  ;  the  diet  should  be  light  and  nutritious,  in  fact 
the  general  measures  which  have  been  previously  recom- 
mended for  the  treatment  of  chronic  mitral  lesions,  and  into 
the  details  of  which  I  need  not  again  enter,  are  appropriate 
here.  The  general  health  must,  at  the  same  time,  be  kept  in 
the  highest  possible  stage  of  efficiency.  A  prolonged  course 
of  arsenic,  given  in  gradually  increasing  doses,  in  accordance 
with  the  capabilities  of  each  individual  patient,  should  be 
tried  ;  this  is  the  only  drug  which  in  my  hands  has  seemed 
to  produce  any  real  and  lasting  benefit  in  chronic  myo- 
carditis. Dr  Roberts  Bartholow  speaks  hopefully  of  small 
doses  of  the  chloride  of  gold  (Vo^h  of  a  grain,  three  times 
daily).  Whenever  symptoms  and  signs  of  cardiac  failure 
arise  they  must  be  met  by  appropriate  remedies,  digitalis, 
alcoholic  stimulants,  etc.  In  cases  of  advanced  fibroid  de- 
generation the  heart  does  not  respond  well  to  digitalis.  In  such 
cases  it  is  often  better  to  rely  upon  alcoholic  and  ammoniacal 
stimulants,  spirits  of  chloroform,  etc.,  rather  than  to  push 
large  doses  of  digitalis,  which,  by  increasing  the  arterial  blood 
pressure,  necessarily  throw  increased  work  upon  the  damaged 
organ. 


576  Diseases  of  the  Heart. 

PARTIAL   ANEURISMS   OF   THE   HEART. 

Definition. — The  term  aneurism  of  the  heart,  which  used 
formerly  to  be  applied  to  cases  in  which  a  cardiac  cavity  was 
dilated  as  a  ivJiole,  is  now  restricted  to  those  cases  in  which 
there  is  a  local  bulging  or  dilatation  of  some  part  of  the  organ. 
These  cases  used  formerly  to  be  described  as /rtr/z^/ aneurisms 
of  the  heart. 

^Etiology. — Aneurisms  of  the  heart  are  either  acute  or 
chronic.     Both  varieties  are  rare. 

Acute  aneurisms  of  the  heart  may  result  from  anything 
which  causes  rapid  local  softening  of  a  limited  portion  of  the 
cardiac  wall.  The  resisting  power  of  the  affected  part  of  the 
heart  is  of  course  weakened,  and  it  dilates  and  sometimes  rup- 
tures under  the  internal  blood  pressure.  Acute  ulcerative 
endocarditis,  acute  localised  myocarditis,  and  acute  softening 
the  result  of  thrombosis  of  the  coronary  artery,  are  the  condi- 
tions which  are  most  likely  to  cause  acute  local  dilatations  of 
this  description.  It  has  also  been  thought  that  abscesses  or 
cysts,  which  have  burst  through  the  endocardium,  may  form 
the  starting  point,  as  it  were,  of  acute  local  dilatations.  Dr 
Wickham  Legg,  in  his  learned  and  exhaustive  Bradshaw  Lec- 
ture on  Cardiac  Aneurisms,  to  which  I  would  refer  the  reader 
for  further  particulars  than  can  be  given  here,  thinks  that  these 
causes  are  possible,  but  not  yet  proved. 

CJironic  aneurisms  of  tJic  heart  are  almost  always  the  result 
of  chronic  myocarditis  (fibroid  degeneration).  Fatty  degenera- 
tion seems  to  be  an  occasional,  though  extremely  rare,  cause 
of  the  condition  ;  Dr  Legg  cites  three  cases  in  which  this 
change  was  found.  In  one  case,  also  quoted  by  the  same 
writer,  the  aneurism  was  of  traumatic  origin,  the  patient 
having  been  stabbed  ten  years  before  death  in  the  region  of  the 
heart ;  a  scar  led  from  the  place  of  the  wound  to  the  apex  of 
the  right  ventricle  ;  a  large  bulging  of  the  cardiac  wall,  which 
had  all  the  characters  of  an  ordinary  aneurism  of  the  left 
ventricle  due  to  disease,  had  formed  at  the  seat  of  the  injury.^ 

'  The  Bradshaw  Lecture  on  Cardiac  Aneurisms.  Medical  Times  and  Gazette, 
Aug.  25,  1S83,  p.  199. 


Fig.  242. — Anewism  of  the  left  ventricle.    (^Natural  size.) 

The  left  ventricle  has  been  opened  in  the  usual  manner;  the  aneurism,  partly  filled  with 
laminated  fihrine,  is  seen  to  be  situated  at  the  apex,  on  the  anterior  surface  of  the  ventricle,  and 
close  to  the  septum 

Copied  by  Professor  Turner's  permission  from  a  specimen  in  the  Anatomical  Museum  of 
the  Edinburgh  University 


MH*s.»lCu«««GLT«ono 


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Fig.  2-13. — Annvrl»m  of  the  left  ventricle.     (Natural  size.") 

A  large  circular  opening  (a)  which  represents  the  orifice  of  the  aneurism,  is  situated  in  the 
septum  a  short  distance  below  the  aortic  segments. 

Copied  by  Professor  Turner's  permission  from  a  specimen  in  the  x^natomical  Museum  of 
the  Edinburgh  University. 


MH.o.«iCi.«Mi«otjr«o?Ei)i«; 


Fig.  m.— Aneurism  of  the  septum  ventriculorum  (the  game  prepn  ration  represented  in  fig.  243),  seen 
from  the  iiitirior  of  the  rlgU  ventricle.     {^Natural  size.) 

The  aneurism  («)  forms  a  large  projection  in  the  cavity  of  the  right  ventricle ;  6,  the 
tricuspid  valve;  c,  the  cavity  of  the  right  auricle.  (Copied  from  a  specimen  m  the  Anatomical 
Museum  of  the  Edinburgh  University,  by  Professor  Tui-ner's  permission.) 

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The  Pathology  of  Cardiac  Aneurisms,         577 

Cardiac  aneurisms  may  occur  at  any  age,  but  are  much 
more  common  in  middle  and  advanced  than  in  early  life. 

Pathology. — In  the  immense  majority  of  cases,  both  acute 
and  chronic,  the  aneurismal  dilatation  is  connected  with  the 
cavity  of  the  left  ventricle.  This  is,  of  course,  only  what  we 
would  expect  when  it  is  remembered  : — (i)  that  the  left  ven- 
tricle is  much  more  frequently  affected  by  acute  ulcerative 
endocarditis,  acute  myocarditis,  and  fibroid  degeneration  than 
any  of  the  other  cardiac  cavities  ;  (2)  that  the  blood  pressure 
in  the  cavity  of  the  left  ventricle  is  very  much  greater  than 
in  any  other  part  of  the  organ.  The  conditions,  therefore,  for 
the  production  of  cardiac  aneurisms  are  met  with  much  more 
frequently,  and  in  a  greater  degree,  in  the  cavity  of  the  left 
ventricle  than  elsewhere. 

The  aneurism  is  most  frequently  situated  at  the  apex  of 
the  left  ventricle,  but  it  sometimes  involves  the  septum  and 
other  parts  of  the  wall  of  the  left  ventricle.  These  appear- 
ances are  beautifully  seen  in  figs.  242,  243,  and  244,  which 
are  copied  from  specimens  in  the  anatomical  museum  of  the 
Edinburgh  University,  and  which  I  am  able  to  represent  by 
Professor  Turner's  kind  permission.  Dr  Legg^  states  that  in 
the  cases  which  he  has  collected,  in  fifty-nine  cases  the  aneurism 
was  situated  at  the  apex,  and  in  thirty-one  at  other  parts  of 
the  left  ventricle.     When  the  aneurism  involves  the  septum,  it 

'  Bradshaw  Lecture  on  Cardiac  Aneurisms,  reported  in  the  Medical  Times  ami 
Cazcttc,  Aug.  25,  1883,  p.  199. 

Description  of  Fig.  24^. 

Section  tlirougli  a  co)nine)icing  aneurism  of  the  left  ventricle. 

[Magnified  about  10  diameters.) 

The  bulging  of  the  cardiac  wall,  which  constitutes  the  aneurism,  is  not  seen  in 
the  section,  which  has  been  flattened  out  in  the  process  of  mounting.  The  cardiac 
wall,  between  c  and/  [i.e.  the  wall  of  the  aneurism)  is  very  much  thinned  ;  and, 
at  this  spot,  the  muscular  fibres  have  almost  entirely  disappeared,  their  place- 
being  occupied  by  fibrous  tissue. 

e,  e,  the  endocardium  at  the  bottom  of  the  aneurism  ;  /,  pericardium  ;  m,  ;//, 
a  thin  layer  of  muscular  fibres  adjacent  to  the  endocardium  ;  in'  m',  muscular 
fibres  in  the  wall  of  the  heart ;  f  fibrous  tissue  ;  a,  artery  in  the  pericardium, 
undergoing  obliterative  endarteritis  (more  highly  magnified  in  fig.  273  ;  v,  v, 
large  blood-vessels  in  the  wall  of  the  heart. 

O    O 


578  Diseases  of  the  Heart. 

projects  into  the  cavity  of  the  right  ventricle,  in  consequence 
of  the  fact  that  the  blood  pressure  in  the  cavity  of  the  left 
ventricle  is  greater  than  that  in  the  right.  Acute  aneurisms 
not  unfrequcntly  involve  the  '  undefended  space,'  as  it  is 
termed, — the  highest  portion  of  the  septum  which  is  destitute 
of  muscular  fibres,  and  which  occupies  the  angle  between  the 
posterior  and  right  segments  of  the  aortic  valve. 

Cardiac  aneurisms  vary  in  size  from  slight  local  bulgings 
up  to  large  tumours,  which  have  been  known  to  attain  almost 
the  size  of  the  heart  itself  In  chronic  aneurisms,  such  as  that 
from  which  the  section  represented  in  figure  245  was  made,  all 
three  la}'ers  of  the  heart  (the  endocardium,  myocardium,  and 
pericardium)  are  usually,  if  not  invariably,  found  in  the  wall  of 
the  sac,  but  the  muscular  fibres  of  the  myocardium  may  be 
completely  replaced  by  fibrous  tissue.  In  acute  aneurisms 
due  to  ulcerative  endocarditis,  the  endocardial  layer  is  want- 
ing. Large  aneurisms  generally  contain  some  laminated 
coagula. 

Symptoms  and  physical  signs. — Aneurisms  of  the  heart  arc 
cither  entirely  latent,  or  attended  by  the  symptoms  and  signs 
indicative  of  chronic  myocarditis.  Large  aneurisms,  which 
are,  it  is  needless  to  say,  of  infinite  rarity,  might  give  rise  to 
increased  dulness  on  percussion,  and  pulsation  in  the  region  of 
the  heart.  Skoda,  quoted  by  Schroetter,^  observed  a  bulging 
of  the  intercostal  spaces  overlying  the  seat  of  an  aneurism. 

Diagiiosis.Sn\dL\\  aneurisms  cannot  of  course  be  recog- 
nised during  life.  An  aneurism,  of  sufficient  size  to  produce 
increased  impulse  and  increased  dulness  on  percussion,  would 
have  to  be  distinguished  from  simple  (general)  dilatation  of 
the  cardiac  cavities  and  from  aneurisms  of  the  aorta.  It  is 
most  improbable  that  any  of  the  readers  of  this  work  will 
meet  with  such  a  case.  The  position  and  outline  of  the  pulsa- 
tion and  dulness,  the  absence  of  any  of  the  ordinary  causes  of 
cardiac  dilatation  (such,  for  example,  as  stenosis  of  the  mitral 
orifice),  would,  I  should  suppose,  be  the  chief  facts   suggestive 

>  Zicinssciis  Cyclopaedia,  vol.  vi.  p.  246; 


Hypertrophy  and  Dilatation  of  the  Heart.     5  79 

of  an  aneurism  of  the  heart ;  the  supposition  would,  of  course, 
he  strengthened  if  the  observer  had,  before  the  appearance  of 
the  physical  signs  suggestive  of  aneurism,  made  the  diagnosis 
of  fibroid  degeneration  of  the  heart.  These  suppositions  are, 
it  is  needless  to  say,  purely  theoretical,  no  such  case  having 
come  under  my  own  personal  observation. 

Prognosis. — The  prognosis  must,  of  course,  be  based  upon 
the  general  condition  of  the  heart,  since  it  is  so  rarely  possible 
to  suspect  the  presence  of  a  cardiac  aneurism.  Cardiac  aneur- 
isms sometimes  rupture,  causing  sudden  or  instantaneous 
death  ;  in  other  cases  the  patient  dies  suddenly  from  syncope. 
Gradual  death  may,  of  course  result  from  the  fatty,  fibroid,  or 
other  cardiac  lesions,  which  happen  to  be  present. 

Treatment. — -The  treatment  is  that  which  has  been  pre- 
viously recommended  for  fibroid  degeneration.  Should  the 
presence  of  a  large  cardiac  aneurism  be  suspected,  the  appro- 
priate treatment  for  aortic  aneurisms  should  be  carried  out. 

HYPERTROPHY   AND   DILATATION   OF   THE   HEART. 

Hypertrophy  and  dilatation  are  closely  related,  and  are 
very  often  met  with  in  combination  ;  hypertrophy,  it  is  true, 
not  unfrequently  occurs  without  dilatation,  but  dilatation,  of 
the  ventricles  at  least,  is  almost  invariably  associated  with 
some  hypertrophy.  Mechanical  causes  play  a  very  important 
part  in  the  production  of  both  conditions  ;  but  the  vital  state 
of  the  organism  as  a  whole,  and  of  the  heart  in  particular,  is 
no  less  important ;  the  rapidity,  too,  with  which  the  mechanical 
causes  to  which  I  shall  presently  refer  more  in  detail,  are 
established,  exerts,  in  many  cases,  a  very  important  influence 
in  determining  the  nature  of  the  result  {i.e.  in  determining 
whether  hypertrophy  or  dilatation  will  result).  An  obstruc- 
tion to  the  passage  of  the  blood  through  the  minute  arteries  of 
the  body,  which  raises  the  arterial  blood  pressure  and  throws 
an  increased  strain  on  the  cavity  of  the  left  ventricle,  is  an 
excellent  example  of  the  mechanical  causes,  which  in  some 
cases  determine  the  production  of  hypertrophy,  and  in  others 


580  Diseases  of  the  Heart. 

of  dilatation.  When  the  organism,  as  a  whole,  and  the  heart 
in  particular,  is  healthy,  and  when  the. obstruction  to  the  blood 
flow  is  slowly  and  gradually  established,  the  increased  stimula- 
tion of  the  cardiac  muscle,  and  the  increased  effort  demanded 
of  it,  result  in  the  production  of  hypertrophy  ;  when,  on  the 
contrar)-,  the  vitality  of  the  organism  as  a  whole  is  below  par, 
when,  more  especiaHy,  the  cardiac  muscle  is  degenerated  or 
otherwise  diseased,  the  heart  does  not  respond  to  the  increased 
stimulation,  and  instead  of  becoming  hypertrophied  and  equal 
to  cope  with  the  obstraction,  its  muscular  wall  yields  under 
the  increased  blood  pressure,  and  dilatation  is  produced. 
When,  again,  a  considerable  obstruction  is  ver}^  rapidly  estab- 
lished there  may  be  no  time  for  the  production  of  h}-pertrophy  ; 
in  such  cases  rapid  or  acute  dilatation  is  produced.  The 
part  of  the  heart,  too,  which  receives  the  strain  and  has  to  put 
forth  the  increased  effort  to  overcome  the  obstruction,  is  a 
point  of  very  great  importance.  The  thick  left  ventricle 
possesses  a  much  greater  degree  of  reserve  force  than  the  thin- 
walled  left  auricle,  hence  its  tendency  to  become  hypertro- 
phied rather  than  dilated  ;  the  auricle,  on  the  contrary,  tends 
to  dilate  rather  than  to  hypertrophy. 

Now  in  a  large  proportion  of  the  cases,  in  which  mechani- 
cal causes  of  hypertrophy  and  dilatation  are  met  with  in  the 
living  man,  the  organism,  as  a  whole,  and  the  heart  in  parti- 
cular, is  not  quite  healthy,  the  response  to  the  increased 
stimulus  is  consequently  imperfect,  and,  while  a  certain 
amount  of  hypertrophy  is  produced,  a  certain  amount  of 
dilatation  is  at  the  same  time  established.  In  many  cases, 
too,  in  which  the  hypertrophy  was  in  the  earlier  stages 
tolerably  perfect,  and  the  dilatation  at  a  minimum,  the 
cardiac  muscle  subsequently  degenerates,  and  the  hyper- 
trophy gives  place  to  dilatation.  All  degrees  of  combina- 
tion are  therefore  met  with,  from  pure  hypertrophy  without 
any  dilatation  on  the  one  hand,  to  extreme  dilatation  with 
hypertrophy  at  a  minimum  on  the  other.  If  this  association 
be  clearly  kept  in  view,  we  may  now  conveniently  consider 
hypertrophy  and  dilatation  separately. 


Varieties  of  Hypertrophy.  581 

HYPERTROPHY    OF    THE    HEART. 

Definition. — Increase  of  the  muscular  wall  of  the  heart,  the 
result  of  increase  of  the  muscular  tissue.  (A  hypertrophied 
heart  is  heavier,  and  almost  always  larger,  than  a  normal 
heart,  but  it  must  be  remembered  that  all  large,  heavy,  and 
thick- walled  hearts  are  not  necessarily  hypertrophied.  In- 
creased thickness  of  the  cardiac  walls  may  be  due  to  deposits 
of  fat,  increase  of  connective  tissue,  or  the  presence  of  new 
growths  (syphilitic  gummata,  cancerous,  or  sarcomatous 
nodules,  etc.)  ;  in  many  cases  of  this  description,  to  which  the 
term  'false'  or  'spurious'  hypertrophy  is  sometimes  applied, 
the  proper  muscular  elements  are  in  places  atrophied,  and  the 
thickened  heart  is  actually  weaker  than  normal.  Increased 
size  of  the  heart  may  also  be  due  to  dilatation  ;  but,  as  I  have 
already  explained,  some  hypertrophy  is  almost  always  present 
in  cases  of  this  description). 

Varieties. — Three  varieties  of  hypertrophy  are  usually 
described,  viz. : — 

(1)  Simple  HypertropJiy. — In  this  form  the  muscular  wall 
of  the  heart,  or  rather  of  the  affected  cavity  of  the  heart,  for 
it  is  seldom  that  all  the  cavities  are  implicated,  is  increa.sed, 
but  the  cavity  itself  is  of  normal  size.  The  left  ventricle  in 
cases  of  cirrhotic  Bright's  disease,  often  exhibits  this  form  of 
hypertrophy  to  perfection.  In  cases  of  long-continued  bron- 
chitis and  emphysema,  I  have  also  seen  the  right  ventricle 
enormously  hypertrophied  without  any  dilatation. 

(2)  Concentric  HypertropJiy. — This  form,  in  which  the  mus- 
cular wall  of  the  heart  is  increased  and  the  cavity  itself 
diminished  in  size  (contracted),  is  probably  identical  with 
that  previously  described  {i.e.  with  simple  hypertrophy).  The 
apparent  diminution  in  the  size  of  the  cavity  is,  in  most  cases, 
if  not  in  all,  a  post  mortem  phenomenon,  and  is  due  to  the  fact 
that  the  heart's  action  was  arrested  in  systole,  and  that  the 
muscular  contraction  and  resulting  obliteration  of  the  cardiac 
cavity  continued  as  the  result  o{  post  mortem  rigidity.  If,  in 
cases  of  this  description,  the  heart  be  steeped  for  a  few  hours 


582  Diseases  of  the  Heart. 

in  warm  water,  so  as  to  render  its  walls  flaccid,  the  cavity 
which  seemed  to  be  obHterated  will  usually  (always  in  my 
experience)  be  found  of  normal  size.  It  is,  in  fact,  extremely 
doubtful  if  concentric  hypertrophy  ever  actually  occurs. 

(3)  Eccentric  HypcrtropJiy. —  In  this  form  the  muscular 
wall  of  the  heart  is  increased,  while  the  cavity  is  at  the 
same  time  dilated.  Eccentric  hypertrophy  is  extremely 
common,  and  is  met  with  in  its  most  typical  form  in  the 
left  ventricle  of  long-continued  aortic  regurgitation.  It  is 
synonymous  with  the  form  of  dilatation  which  is  technicall}- 
tcrmed  dilatation  zvith  Jiypcrtrophy,  in  contradistinction  to 
siinp/c  dilatation. 

yEtioIogy  and  Pathology — In  some  cases  the  hypertrophy- 
is  general,  and  involves,  more  or  less,  all  four  cavities  of  the 
heart ;  more  commonly  it  is  limited  to  one  or  two  cavities  ; 
the  ventricles  are  affected  much  more  frequently  than  the 
auricles,  and  the  cavities  on  the  left  side  of  the  heart  than 
those  on  the  right ;  the  order  of  relative  frequency  with 
which  the  four  cardiac  cavities  are  affected  is  therefore  : — 

Left  ventricle. 
Right  ventricle. 
Left  auricle. 
Right  auricle. 

It  is  a  disputed  point,  whether  in  cases  of  cardiac  hyper- 
trophy there  is  an  actual  increase  in  the  number  of  the 
muscular  elements,  or  whether  the  original  muscular  fibres 
are  simply  increased  in  size.  The  question  is  one  which  is 
not  of  any  great  practical  importance,  I  need  not,  therefore, 
enter  into  details,  suffice  it,  however,  to  say,  that  both  altera- 
tions probably  occur. 

Speaking  generall}-,  it  may  be  said  that  the  cause  of 
hypertrophy  of  the  heart  is  increased  stimulation  and 
over- work.  In  the  great  majority  of  cases,  the  primary 
cause  is  mechanical,  such,  for  example,  as  obstruction  to 
the  blood-flow  either  inside  or  outside  the  organ.  Hyper- 
trophy seems  also  sometimes  to  be  caused  by  long-continued 


Aitiology  of  Hypertrophy  of  the  Heart.        583 

over-activity,  the  result  of  neurotic  or  other  conditions,  in- 
dependently of  obstruction  to  the  blood-current  or  other 
mechanical  causes. 

It  is  extremely  important  to  remember  that  for  the  pro- 
duction of  satisfactory  hypertrophy  the  cardiac  muscle  must 
be  healthy,  and  the  conditions  for  its  nutrition  satisfactory. 
When,  for  instance,  the  muscular  fibres  are  degenerated,  the 
heart  may  be  incapable  of  becoming  hypertrophied,  as  in  the 
case  of  cirrhosis  of  the  kidney  and  fibroid  degeneration  of 
the  heart,  which  I  have  previously  described.  So  again,  when 
the  arterial  blood  supply  to  the  cardiac  walls  is  insufficient  in 
consequence  of  disease  of  the  coronary  arteries,  or  when  the 
v\^aste  products  of  combustion  are  retained  in  the  heart  in 
consequence  of  venous  congestion,  the  hypertrophy  is  imper- 
fect, or,  if  it  should  have  been  previously  established,  gives 
place  to  dilatation  in  consequence  of  fibroid  or  fatty  changes 
in  the  thickened,  and,  at  the  same  time,  imperfectly  nourished 
muscular  walls  of  the  organ. 

The  chief  causes  of  hypertrophy  are  therefore  as  follows  : — 

A.  Extrinsic  causes. 
\.  Long-co}itiniicd  simple  over-activity  or  fimctional  excite- 
inent. — Under  this  head  are  included  those  cases  of  hyper- 
trophy of  the  heart  which  result— ((^)  from  physiological  over- 
activity, such  as  is  necessitated  by  violent  muscular  eff'ort  ; 
{b)  from  long-continued  neurotic  palpitation  due  to  any 
cause,  such  as  exophthalmic  goitre,  sexual  excesses  or  irre- 
gularities, etc.  The  occurrence  of  cases  of  this  description, 
which  are  sometimes  called  cases  of  ' idiopattiic'  hypertrophy, 
is  doubted  by  some  observers  ;  but  while  allowing  that  they 
are  seldom  seen  on  the  post  viorteni  table,  for  the  conditions 
with  which  they  are  associated  are  rarely  fatal,  I  am  perfectly 
convinced,  from  the  clinical  examination  of  living  patients, 
that  they  do  actually  occur.  In  these  cases  the  hypertrophy 
is,  as  a  rule,  gcnei-al,  i.e.  it  involves  both  the  left  and  the  right 
hearts. 

2.  Obstmctiou  to  tJie  btood-ftoiv  outside  tite  Jieai't. — This  is 
an  extremely  common  cause  of  hypertrophy  both  of  the  left 
and  of  the  right  ventricles.     Any  obstruction,  for  examj^le,  to 


584  Diseases  of  the  Heart. 

the  passage  of  the  blood  through  the  systemic  arterial  system 
will,  if  long  continued,  produce  hypertrophy  of  the  left  ven- 
tricle ;  while,  hypertrophy  of  the  right  ventricle  follows  an}- 
long-continued  obstruction  in  the  pulmonary  circuit.  The 
different  pathological  conditions,  which  produce  hypertrophy 
of  the  left  and  right  ventricles,  and  which  are  included  under 
this  head,  will  be  presently  detailed.  In  cases  of  this  descrip- 
tion the  hypertrophy  is,  in  many  cases,  pure,  i.e.  unassociated 
with  dilatation. 

3.  Obstruction  to  the  blood-flow  in  the  heart  itself. — This, 
too,  is  one  of  the  most  common  causes  of  cardiac  hypertrophy. 
The  cavity,  which  is  situated  immediately  behind  the  obstruc- 
tion, becomes  first  hypertrophied  ;  in  the  case  of  aortic  sten- 
osis, for  example,  the  left  ventricle  is  first  affected,  in  the 
case  of  mitral  stenosis  the  left  auricle,  and  so  on. 

4.  Increased  distention  of  a  cardiac  cavity.  —  When,  for 
example,  the  left  ventricle  receives  an  unusually  large  quan- 
tity of  blood,  as  it  does  in  cases  of  aortic  and  mitral  regurgi- 
tation, its  muscular  wall  is  unduly  stimulated,  and  an  increased 
effort  is  required  to  empty  it ;  hypertrophy  is  in  consequence 
produced.  In  cases  of  this  description  the  hypertrophy  is 
always  combined  with  dilatation. 

5.  An  iuipedinient  to  the  free  contraction  of  t/u^  heart,  such 
as  is  present  in  some  cases  of  adJieroit  pericardium. — Cases  of 
adherent  pericardium  are  not  unfrequently  met  with,  in  which 
the  heart  is  hypertrophied  ;  in  many  of  these  cases,  the  hyper- 
trophy is  due  to  associated  valvular  disease  ;  but  in  some, 
it  is,  I  think,  in  part  at  least,  due  to  the  impediment  to 
the  free  action  of  the  organ,  which  is  caused  by  the  peri- 
cardial adhesions.  The  heart  is  most  likely  to  become 
hypertrophied  when  the  pericardium  is  adherent  to  the 
chest-wall  on  the  one  hand,  and  to  the  exterior  of  the 
heart  on  the  other.  When  extensive  pericardial  adhesions 
of  this  description  are  present,  there  is  often  at  the  same  time 
extensive  fibroid  degeneration  of  the  myocardium.  In  such 
cases  the  cardiac  muscle  may  be  so  extensively  degenerated 
as  to  be  incapable  of  responding  to  the  extra  exertion  de- 
manded of  it.     In  fact,  in  many  cases  of  adherent  pericardium 


The  ^Etiology  of  Hypertrophy  of  the  Heart.     585 

the  muscular  tissue  of  the  heart  is  more  or  less  atrophied  ; 
and  it  is  in  cases  of  this  description,  in  which  the  walls  of 
the  heart  are  often  much  thickened,  that  a  careless  observer 
is  likely  to  mistake  the  '  spurious '  or  '  false '  hypertrophy  for 
the  '  true '  form  of  the  condition. 

Let  us  now  consider  the  hypertrophies  of  the  left  and  right 
hearts,  and  of  the  individual  cavities  in  detail.  This  division 
of  the  subject  has  many  practical  advantages,  and  is  amply 
justified  by  the  results  of  clinical  and/(?-sY  jnorteni  observation. 
It  must,  however,  be  remembered  that  hypertrophy  of  either 
heart  is  very  generally  associated  with  some  hypertrophy  of 
the  other.  The  affection  of  both  hearts  is  sometimes  due  to 
the  fact,  that  the  original  cause  of  the  hypertrophy,  although 
situated  in  one  heart,  ultimately  throws  an  increased  strain 
on  the  other.  Aortic  regurgitation,  for  example,  first  causes 
hypertrophy  of  the  left  ventricle,  but  ultimately  causes  such 
engorgement  of  the  pulmonary  circulation,  that  hypertrophy 
of  the  right  ventricle  is  produced.  So,  too,  great  obstruction 
originating  in  the  lungs,  as  in  cases  of  long-continued  bron- 
chitis and  emphysema,  first  produces  hypertrophy  of  the  right 
heart,  but  ultimately  may  cause  some  hypertrophy  of  the  left 
ventricle,  in  consequence  of  the  difficulty  which  the  arteries 
have  in  emptying  themselves  into  the  greatly  engorged  and 
now  distended  veins.  The  subcutaneous  dropsy  which  is 
usually  present,  also  mechanically  impedes  the  systemic  peri- 
pheral circulation.  Further,  the  venous  condition  of  the  blood 
adds  to  the  difficulties  of  the  arterial  circulation,  firstly,  by 
causing  increased  capillary  resistance,  for  venous  blood  passes 
with  difficulty  through  the  capillary  vessels,  and  secondly,  by 
stimulating  the  vaso-motor  centre,  and  producing  contraction 
of  the  minute  arteries. 

Probably,  too,  it  is  impossible  to  have  much  hypertrophy 
of  one  ventricle  without  some  hypertrophy  of  the  other,  in 
consequence  of  the  fact  that  the  two  ventricles  are  in  the 
habit  of  acting  harmoniously  together,  and  that  the  tissues 
of  the  one  are  to  some  extent,  at  least,  continuous  with  the 
tissues  of  the  other.  In  a  case,  which  recently  came  under 
my  obser\'ation  in  the  post-nwiicvi  theatre,  in  which  the  right 


586  Diseases  of  the  Heart. 

heart  was  enormously  hypertrophied  in  consequence  of  long- 
continued  bronchitis  and  emphysema,  it  seemed  difficult  to 
account  for  the  great  hypertrophy  of  the  left  ventricle,  which 
was  also  present,  on  any  other  supposition. 

IIYPERTROPIIV   OF   THE   LEFT   VENTRICLE. 

ALtiology.—Th^  left  ventricle  is  the  part  of  the  heart 
which  is  most  prone  to  hypertrophy.  The  chief  clinical  and 
pathological  conditions  which  produce  hypertrophy  of  the  left 
ventricle  are  as  follows  : — 

A.  Intrinsic  causes — i.e.  conditions  within  the  left  heart.^ 
(i)  Aortic  Stenosis. — In  this  condition,  the  hypertrophy  is 
as  a  rule  '  simple,'  i.e.  there  is  little  or  no  associated  dilatation. 
The  hypertrophy  results  from  the  increased  effort  which  is 
required  to  force  the  blood  through  the  narrowed  aortic 
orifice. 

(2)  Aortic  Regurgitation. — Here  the  hypertrophy  is  of  the 
'eccentric'  variety  ;  the  associated  dilatation  is  often  consider- 
able, and  the  hypertrophy  great ;  in  fact  it  is  in  cases  of  aortic 
regurgitation  that  the  largest  and  heaviest  hearts  occur.  It 
was  stated  recently  in  one  of  the  medical  journals  (I  have 
unfortunately  lost  the  reference),  that  a  heart  was  shown  to 
the  IMedical  Society  of  New  York  which  weighed  no  less 
than  57  ounces.  Dr  Bristowe  has  recorded  another  which 
weighed  46^  ounces,  and  I  myself  have  met  with  an  example 
(the  case  detailed  on  page  501)  in  which  the  weight  of  the 
heart  was  45  ounces.  When  the  aortic  valve  is  incompetent, 
blood  is  poured  into  the  cavity  of  the  left  ventricle  during  the 
ventricular  diastole  from  two  sources,  viz.,  from  the  aorta  on 
the  one  side,  and  from  the  left  auricle  on  the  other ;  the 
forcible  distention  of  the  cavity,  the  walls  of  which  are  flaccid, 
produces,  from  the  first,  some  dilatation  ;  the  muscular  wall 
of  the  cavity  is  more  forcibly  and  more  frequently  stimulated 
than  in  health  ;  and  there  is  at  the  same  time  an  unusually 
large  quantity  of  blood  to  be  discharged.     These  conditions 


'   It  will  be  observed  that  I  use  the  terms  'extrinsic'  and  'intrinsic'  as  applied 
to  the  left  heart,  and  not  to  the  heart  as  a  whole. 


Aitiology  of  Hypertrophy  of  the  Lejc  y  en t ride.  587 

(excessive  stimulation  and  the  increased  effort  req^uired  to 
expel  the  abnormally  large  contents)  necessarily  lead  to 
hypertrophy. 

(3)  Mitral  incompetence. — In  free  mitral  regurgitation  the 
left  ventricle  is  almost  always  increased  in  thickness  ;  the 
hypertrophy  being  of  the  '  eccentric '  variety,  i.e.  associated 
with  some  dilatation.  (In  some  cases  the  hypertrophy  is  of 
the  '  spurious  '  or  '  false  '  form,  but  in  most  cases  true  hyper- 
trophy is  present).  Considerable  difference  of  opinion  has 
existed  as  to  the  manner  in  which  the  hypertrophy  is  pro- 
duced in  cases  of  this  description,  {a)  The  chief  cause  is,  I 
believe,  excessive  stimulation  of  the  muscular  wall,  and  the 
increased  effort  which  is  required  to  expel  the  abnormally 
large  quantity  of  blood  which  the  cavity  contains.  In  cases 
of  free  mitral  regurgitation  the  left  auricle  and  the  whole  pul- 
monary circuit  are  greatly  distended  during  the  ventricular 
systole  ;  as  soon  as  the  contraction  of  the  left  ventricle  ceases, 
the  mitral  valve  yields  before  blood  pressure,  and  an  unusual  1)' 
large  quantity  of  blood  passes  with  great  force  into  the  left 
ventricle,  the  walls  of  which  are  in  a  flaccid  and  relaxed  con- 
dition. Some  dilatation  of  the  left  ventricle  is  consequently 
produced,  its  muscular  wall  is  more  forcibly  and  frequently 
stimulated  than  in  health,  and  an  increased  effort  is  required 
to  expel  its  abnormally  large  contents  ;  hence  the  production 
of  hypertrophy.  But  whilst  this  is  the  main  cause,  the  hyper- 
trophy is  probably  in  part  due  to  the  fact  {b)  that  the  left 
ventricle  shares  in  the  hypertrophy  of  the  right  heart,  which 
is  present  (this  point  has  been  previously  referred  to  on  page 
585) ;  possibly,  too,  in  the  later  stages  of  mitral  disease,  to 
(r)  the  difficulty  which  is  offered  to  the  passage  of  the  blood 
from  the  systemic  arterial  system  into  the  engorged  veins. 
(This  cause  of  hypertrophy  has  also  been  explained.  See 
page  585.)  The  hypertrophy  of  the  left  ventricle,  which  is 
met  with  in  some  cases  of  mitral  stenosis  (in  which  the  left 
ventricle  is,  as  a  rule,  of  normal  size,  or  smaller  than  normal) 
is  probably  also  produced  in  the  manner  described  under  the 
two  latter  heads  {b  and  r). 

(4)  Pericarditis,  ivitli  extensive  adiiesions. — There  is  seldom 


5 88  Diseases  of  the  Heart. 

much  true  hypertrophy  of  the  left  ventricle  in  such  cases. 
(The  manner  in  which  pericardial  adhesions  may  produce 
cardiac  hypertrophy  has  already  been  described.  See  page 
584.) 

B.  Extrinsic  Causes — {i.e.  causes  outside  the  left  heart.) 
I.  Bright s  Disease  of  the  Kidney. — Hypertrophy  of  the 
left  ventricle  is  seen  in  all  forms  of  Bright's  disease  (the  waxy 
or  lardaceous,  when  uncombined  with  cirrhosis,  excepted),  but 
reaches  its  highest  degree  in  the  cirrhotic  variety.  In  cases  of 
this  description,  there  is  little  or  no  dilatation,  i.e.  the  hyper- 
trophy is  of  the  '  simple '  ^  variety.  \''arious  theories  have 
been  advanced  to  account  for  the  hypertrophy  of  the  left 
ventricle  which  is  so  constantly  present  in  cirrhotic  Bright's 
disease.  All  observers  are  agreed  firstly,  that  the  cause  of 
the  hypertrophy  is  situated  outside  the  heart,  i.e.  in  some  part 
of  the  arterial  or  capillary  systems  ;  secondly,  that  in  conse- 
quence of  this  obstruction  in  the  arterial  or  capillary  system 
of  vessels,  the  arterial  blood  pressure  is  increased  ;  and  thirdly, 
that  the  left  ventricle  has  consequently  more  work  to  do,  and 
therefore  becomes  hypertrophied.  But  opinions  differ  as  to 
the  exact  manner  in  which  the  obstruction  is  produced. 

Tranbe  believed  that  the  increased  arterial  tension  re- 
sulted from  the  difficulty  which  the  blood  meets  with  in 
passing  through  the  cirrhosed  kidneys,  a  part  of  the  capillary 
.system  of  the  kidneys  being  cut  off,  as  it  were,  by  the  fibroid 
lesion. 

Sir  William  Gull  and  Dr  Sutton  suppose  that  the  cirrhosis 
of  the  kidney  is  only  part  and  parcel  of  a  vascular  lesion, 
arterio-capillary  sclerosis,  as  they  term  it,  which  is  distributed 
throughout  the  whole  body  ;  and  that  the  increased  arterial 
tension  is  due  to  the  difficulty  which  the  blood  meets  with 
in  passing  through  the  minute  arteries  and  capillaries,  the 
calibre  of  which  is  narrowed  by  the  fibro-hyaloid  change 
which  they  claim  to  have  demonstrated. 

*  I  do  not  refer  to  the  '  concentric '  form,  which  i.s,  I  believe,  an  unreal  form  ; 
it  is,  however,  in  cases  of  '  contracted  '  kidney  that  this  supposed  concentric 
hypertrophy  is  most  frequently  observed. 


Aitiology  of  Hypertrophy  of  the  Left  Ventricle.  589 

Dr  George  Johnson  thinks  that  in  consequence  of  the 
kidney  affection,  excrementitious  products,  urea  and  its  com- 
pounds, are  retained  in  the  blood  ;  that  the  muscular  coats  of 
the  minute  arteries  are  irritated  and  kept  in  a  spasmodic  state 
of  contraction,  and  become  hypertrophied  ;  and  that  in  con- 
sequence of  these  arterial  changes  the  calibre  of  the  minute 
arteries  throughout  the  body  is  narrowed,  the  arterial  tension 
increased,  and  an  increased  strain  thrown  upon  the  left 
ventricle. 

Dr  Broadbent  is  of  opinion  that,  while  contraction  of  the 
arterioles  may  give  rise  to  very  high  arterial  tension,  and  no 
doubt  often  co-operates  with  capillary  resistance  in  its  pro- 
duction, the  seat  of  the  obstruction  from  which  high  pressure 
within  the  arterial  system  usually  arises,  is  situated  in  the 
capillary  system  of  vessels.^ 

Space  does  not  permit  me  to  discuss  in  detail  the  various 
facts  and  arguments  which  have  been  brought  forward  in 
support  of  these  different  views.  Suffice  it  to  say,  that  I 
agree  with  those  who  think  firstly,  that  the  primary  cause  is 
the  kidney  lesion  ;  secondly,  that  in  consequence  of  the  kidney 
lesion  the  blood  becomes  loaded  with  excrementitious  matters, 
and  that  it  is  owing  to  the  presence  of  these  impurities  in  the 
blood  that  the  increased  arterial  tension  is  produced.  It  is 
much  more  difficult  to  decide  the  third  step  in  the  process, 
and  to  determine  the  exact  manner  in  which  the  increased 
arterial  tension  is  brought  about,  i.e.  whether  it  is  due  to 
increased  capillary  resistance  or  to  obstruction  in  the  minute 
arterioles  ;  probably  both  views  are  correct.  So  far  as  I  can 
weigh  the  facts,  I  am  disposed  to  think  that  the  chief  cause 
of  the  obstruction  must  be  in  the  minute  arteries.  At  the 
same  time  I  am  quite  willing  to  allow  that  impure  blood 
probably  passes  through  the  capillaries  with  greater  difficulty 
than  healthy  blood.  I  am  disposed,  therefore,  to  think  that 
the  increased  arterial  tension  of  cirrhotic  Bright's  disease  is 
due,  partly  to  increased  capillary  resistance,  partly  and  chiefly 
to  increased  contraction  of  the  minute  arteries.  The  over- 
contraction  of  the  arteries,  or  arterial  spasm,  as  it  has  been 

•  British  Medical Jour7nil,  Aug.  25,  1S83,  p.  357. 


590  Diseases  of  tJie  Hea/'t. 

termed,  is  possibly  produced  by  the  direct  irritation  of  urea 
and  its  products,  possibly,  as  Ludvvig  has  supposed,  by  the 
action  of  the  retained  urinary  products  on  the  vaso-motor 
centre.  Perhaps,  too,  it  may  be  partly  caused,  as  Israel  and 
Grawitz  (quoted  by  Dr  Saundby  in  the  debate  on  increased 
arterial  tension  at  the  Liverpool  Meeting  of  the  British 
Medical  Association  ^),  by  the  direct  action  of  the  retained 
urinary  products  on  the  cardiac  ganglia  or  muscle  of  the 
heart.  (These  observers  have  shown  that  high  arterial  tension 
may  be  produced  by  feeding  animals  on  urea.  It  is  interesting 
in  this  connection  to  remember  the  close  relationship  which, 
as  Gaskcll  and  others  have  shown,  the  cardiac  muscle  bears  to 
unstriped  muscular  fibre,  and  the  fact  that  some  substances, 
e.g.  digitalis,  which  stimulate  the  muscular  fibre  of  the  heart, 
also  act  upon  the  muscular  coats  of  the  arteries.  It  is  highly 
probable,  therefore,  that  if  urea  directly  stimulates  the  cardiac 
muscular  fibre,  it  also  directly  stimulates  the  muscular  coat 
of  the  minute  arteries-^an  additional  argument  to  the  others 
which  can,  I  think,  be  legitimately  advanced  to  show  that  the 
contraction  of  the  arterioles  exercises  a  very  important,  I 
would  say,  the  most  important  part,  in  the  production  of  the 
high  arterial  tension  of  Bright's  disease.) 

2.  Atheroma. — All  observers  agree  that  a  rigid  inelastic 
condition  of  the  arteries  causes  a  decided  obstruction  to  the 
blood  current,  and  throws  an  increased  strain  on  the  left  ven- 
tricle, which  tends,  therefore,  to  become  hypertrophied.  In 
some  cases  of  this  description,  the  cardiac  muscle  is  fatty  or 
otherwise  degenerated,  and  incapable  of  much  hypertrophy  ; 
dilatation  then  of  course  results. 

3.  Constriction  of  the  aorta  or  large  b/ood-vesseIs.~ThQ 
thoracic  aorta  is  sometimes  constricted  as  the  result  of  con- 
genital malformation  (the  constriction  is  usually  situated  just 
beyond  the  ductus  arteriosus  Botalli)  ;  and  in  these  cases 
the  left  ventricle  has  been  found  hypertrophied.  Spinal 
curvatures  and  intra-thoracic  tumours,  which  press  upon 
and  constrict  the  aorta  or  its  large  branches  as  they  leave 
the    narrow  upper   outlet    of  the    thoracic   cavity,   may  also 

'  Reported  in  the  British  Medical  Journal  for  Aug.  25.  1883,  p.  361. 


Symptoms  of  HypertropJiy  of  the  Left  Ventricle.    591 

act  as  mechanical  causes  of  hypertrophy  of  the  left  ventricle. 
Obstruction  of  the  abdominal  aorta  may  also  have  the  same 
effect.  The  influence  which  aneurismal  dilatations  of  the 
aorta,  more  especially  saccular  aneurisms,  have,  in  causing 
hypertrophy  of  the  left  ventricle,  is  doubtful ;  theoretically  we 
would  expect  hypertrophy  to  be  produced,  more  particularly 
in  cases  of  general  dilatation  ;  in  some  cases  it  certainly  does 
occur,  but  not  in  all.  It  is  frequently  absent  when  the  aneur- 
ism is  saccular. 

4.  Pregnancy. — The  hypertrophy  due  to  this  cause  is  so 
well  known  as  to  need  no  comment. 

5.  Chlorosis  and  progressive  pernicious  auceniia. — In  these 
conditions,  arterial  tension  is  usually  increased,  partly,  I  believe, 
in  consequence  of  the  difficulty  with  which  anaemic  blood 
passes  through  the  systemic  capillaries,  partly  because  of 
the  contracted  condition  of  the  minute  arteries,  produced  by 
stimulation  of  the  vaso-^motor  centre.  (Physiologists  have 
shown  that  the  vaso-motor  centre  is  stimulated  not  so  much 
by  an  excess  of  carbonic  acid  in  the  blood  as  by  a  deficiency 
of  oxygen.) 

6.  Pulmonary  lesions  (such  as  emphysema  and  cirrhosis) 
and  lesions  of  the  right  heart.  —  In  long^continued  cases  of 
this  description  the  left  ventricle  may  ultimately  become 
hypertrophied.  The  exact  mode  of  causation  has  been  pre- 
viously described.     (See  page  5^^5-) 

Synptonis  and  consequences  of  hypertrcphy  of  the  left  ven- 
tricle.— In  considering  the  symptoms  and  consequences  of 
hypertrophy  of  the  left  ventricle,  it  must  always  be  remem- 
bered, that  in  the  great  majority  of  cases  the  condition  is 
secondary,  and  that  it  is  for  the  most  part  a  salutary 
change. 

The  hypertrophy  itself  may  produce  no  discomfort  to  the 
patient ;  and  even  when  it  does  produce  symptoms,  they  are 
almost  always  secondary  and  subordinate  to  those  which 
result  from  the  primary  lesion.  The  symptoms,  which  may 
result  from  the  hypertrophy  itself,  are  : — consciousness  of  the 
action  of  the  heart  (uneasiness,  a  feeling  of  distention  in  the 


592  Diseases  of  tJie  Heart. 

precordial  region,  intermittent  action,  and,  above  all,  palpita- 
tion) ;  shortness  of  breath  ;  symptoms  due  to  over-distention 
of  the  vessels,  such  as  throbbing  of  the  arteries,  fulness  of  the 
heart,  headache,  flushings,  noises  in  the  ears,  flashes  before  the 
eyes,  etc.  Palpitation  is  very  common  in  the  advanced  stages 
of  hypertrophy,  and  is  suggestive  of  commencing  dilatation  ; 
it  indicates,  as  a  rule,  that  the  enlarged  heart  is,  in  conse- 
quence of  degenerative  (fibroid  or  fatty)  changes,  unable  to 
cope  with  this  obstacle  in  front ;  or,  to  use  the  expressive 
words  of  Dr  Fothergill,  '  palpitation  is  the  outward  visible 
sign  of  internal  incompetence.'^ 

The  injurious  results  which  may  follow  hypertrophy  of  the 
left  ventricle  are  atheroma  and  aneurismal,  or  simple  dilatation 
of  the  arteries,  and  arterial  rupture.  These  results  do  not,  of 
course,  always  occur  ;  they  are  only  likely  to  be  produced  in 
those  cases  in  which  an  excessive  quantity  of  blood  is  pro- 
pelled by  the  hypertrophied  left  heart  into  the  arterial  system. 
They  are  most  likely  to  occur  in  atheroma,  in  kidney 
disease,  and  in  those  cases  of  aortic  incompetence  in  which 
there  is  no  obstruction  at  the  aortic  orifice.  In  cases  of  this 
description,  the  force  of  the  hypertrophied  left  ventricle  is,  as 
it  were,  expended  on  the  arterial  system,  and  if  the  arteries 
are  degenerated,  aneurism  and  rupture  may  of  course  arise. 
We  know,  too,  that  sudden  and  forcible  distention  of  the 
arteries,  when  long  continued,  is  a  fertile  source  of  atheroma. 
Long  continued  and  forcible  over-distention  of  the  arterial 
system  (such  as  is  met  with  in  some  cases  of  cardiac  hyper- 
trophy), may,  therefore,  lead  to  the  formation  of  aneurisms 
and  to  arterial  ruptures,  firstly,  by  causing  arterial  degenera- 
tion {i.e.  atheroma),  and  secoid/y,  by  causing  the  degenerated 
and  weakened  vessel  to  dilate  or  give  way. 

In  those  cases  of  hypertrophy,  on  the  other  hand,  in  which 
the  force  of  the  left  ventricle  is  not  expended  on  the  arterial 
.system,  as  for  example,  in  stenosis  of  the  aortic  orifice  and 
incompetence  of  the  mitral,  these  injurious  consequences  do 
not  occur.  In  aortic  stenosis,  the  hypertrophy  of  the  left 
ventricle   is   altogether  salutary ;    in    mitral    incompetence,  it 

'  Diseases  of  the  Heart,  V.  127. 


Physical  signs  of  Hypertrophy  of  tJie  L  eft  Ventricle.   593 

is  not  altogether  beneficial,  for  the  greater  the  force  with  which 
the  regurgitant  current  is  driven  backwards  through  the  mitral 
orifice,  the  greater  will  be  the  dilatation  of  the  left  auricle  and 
the  engorgement  of  the  parts  behind  it,  other  things,  more 
particularly  the  extent  of  the  mitral  leak,  being  equal. 

Physical  signs. — The  physical  signs  which  are  met  with  in 
cases  of  hypertrophy  of  the  left  ventricle  vary  with  the  nature 
of  the  primary  lesion  on  which  the  hypertrophy  depends. 
When  the  hypertrophy  is  due  to  mitral  regurgitation  or 
aortic  incompetence,  for  example,  the  primary  physical  signs, 
as  I  term  them,  of  those  lesions  will  be  present,  in  addition  to 
those  which  result  from  the  hypertrophy. 

The  physical  signs  characteristic  of  hypertrophy  of  the 
left  ventricle  per  se  {i.e.  the  primary  physical  signs  of  hyper- 
trophy, as  they  may  be  termed)  are  the  physical  results  of  an 
enlarged  and  forcibly  contracting  left  heart.  It  must,  how- 
ever, be  remembered  that  these  physical  signs  are  not  invari- 
ably present,  for  if  the  enlarged  and  forcibly  acting  left 
ventricle  is  extensively  covered  by  lung,  as  it  is,  for  example 
in  pulmonary  emphysema,  the  physical  indications  may  not  be 
apparent. 

The  apex  beat  is  displaced  do\\nwards  and  outwards,  and 
may  be  situated  in  the  sixth,  seventh,  or  even  the  eighth  inter- 
space, one,  two,  or  even  three  inches  outside  the  line  of  the 
nipple.  (See  fig.  246.)  (When  the  apex  is  much  displaced 
the  heart  is  usually  dilated  as  well  as  hypertrophied.) 

The  impulse  of  the  heart  is  more  forcible  than  in  health 
and  in  many  cases  the  front  wall  of  the  chest  is  forcibly  raised 
up,  as  it  were,  en  masse.  The  contraction  of  the  organ,  and 
therefore  the  impulse,  are  often  more  deliberate  than  in  health. 
A  double  impulse  or  shock  is  sometimes  perceptible,  the  first 
and  chief  impulse  corresponding  to  the  systole  of  the  ventricle, 
the  second  and  weaker  impulse  to  the  closure  of  the  aortic 
segments  and  to  the  cardiac  rebound. 

The  praecordial  region  is,  in  some  cases  (more  especially  in 
children  and  young  persons  in  whom  the  chest-wall  is  soft 
and  yielding),  more  prominent  than  in  health. 

P  P 


594 


/)/src7srs  of  flic   fJcart. 


The  areas  of  cardiac  diilncss,  both  superficial  and  deep 
are  increased,  and  the  percussion  resistance  is  greater  than  in 
health.  In  hypertrophy  of  the  left  ventricle  the  cardiac 
dulness  is  increased  in  the  vertical,  and  to  some  extent 
also  in  the  transverse  directions,  for  the  hypertrophy  is 
usually,  as  I  have  previously  pointed  out,  associated  with 
some  dilatation.     (See  fig.  246.) 


Fi( ; .   7.d,b.— Hype7-tropliy  ofl/tc  lefl  veiilrich-,  showiii^  l/ie  altered  position  of  the  apex. 
— ( .4ftc7-  von  Diisih. ) 

The  continuous  line  represents  the  normal  heart ;  the  dotted  line  the  hyper- 
trophied  left  ventricle.  The  apex  of  the  left  ventricle  is  outside  the  dotted  line 
a  1),  which  is  drawn  through  the  left  nipple. 


Physical  signs  of  Hypertrophy  of  tJic  Left  Ventricle.  595 


The  character  of  thi'  heart  sounds  depends  more  parti- 
cularly upon  the  nature  of  the  primary  lesion.  When  the 
hypertrophy  depends  upon  extra-cardiac  conditions,  i.e.  when 
there  is  no  valvular  disease,  and  when  the  heart  is  (except- 
ing" the  hypertrophy  of  the  left  ventricle)  otherwise  healthy, 
the  impulse  of  the  hypertrophied  heart  can  sometimes  be 
heard  against  the  chest-wall  as  a  jar  or  click  ;  the  first 
sound  is  usually  more  prolonged,  more  muffled  and  duller 
than  in  health,  and  not  unfrequently  reduplicated  ;  when 
the  hypertrophy  is  combined  with  dilatation,  the  first  sound 
is,  on  the  contrary,  louder  and  shorter  than  natural ;  the  aortic 
second  sound  is,  as  a  rule,  loud  and  accentuated.'  When 
the  hypertrophy  depends  upon  intra-cardiac  causes,  such  as 
aortic  or  mitral  disease,  the  sounds  are,  of  course,  modified 
in  accordance  with  the  nature  of  the  valvular  lesion. 

The  character  of  the  cardiographic  tracing. — The  systolic 
portion  of  the  tracing  is  very  prominent,  the  summit  being 
broad  and  sustained,  and  the  eminence,  /",  well  marked. 
(See  figs.  247  and  248.) 


Fk;.  247. 


Fig.  24S. 


Fig.  247.  —  Cardiograpliic  tracing  in  hypertrophy  of  the  left  ventricle.     [Afte? 

Galabin. ) 

'  Emily  L. ,  ctt.  8.  Loud  systolic  murmur  at  the  apex,  preceded  by  a  very  faint 
rumbling  sound.  A  presytolic  murmur  has  been  heard  previously.  Heart  much 
hypertrophied,  P.  96.'     {Guyi's  Hospital  Reports,  1875,  p.  313.) 

Fig.  248.  —  Cardiographic  tracing  in  hypertrophy  of  the  left  ventricle. — (After 

Galabin. ) 

'Thomas  G.,  let.  56.  Chronic  Bright's  disease  with  atheromatous  arteries. 
The  cardiac  impulse  was  very  powerful,  but  no  murmur  was  heard,  I'.  63.' — (Guys 
Hospital  Reports,  1875,  p.  312.) 


596 


Diseases  of  the  Heart. 


The  character  of  the  pulse  also  varies  in  accordance  with 
the  cause  of  the  hypertrophy.  When  the  hypertrophy  is  due 
to  extra-cardiac  conditions,  such  as  cirrhotic  Bright's  disease, 
the  pulse  is  firm,  strong,  and  sustained  ;  sometimes  full  and 
large,  but  more  frequently  of  normal  volume  or  contracted. 
When  the  hypertrophy  depends  upon  intra-cardiac  condi- 
tions, the  character  of  the  pulse  is  variously  modified  in 
accordance  with  the  special  nature  of  the  valvular  lesion.^ 
The  heart's  action,  and  therefore  the  pulse,  is,  as  a  rule, 
regular ;  and  in  this  respect  there  is  a  striking  difference 
between  cases  of  typical  hypertrophy  and  cases  of  typical 
dilatation  ;  in  the  latter  condition  marked  irregularity  is 
frequently  present. 

The  character  of  the  sphygmographic  tracing  depends 
upon  the  condition  of  the  valvular  apparatus  of  the  heart  and 
to   a    considerable   extent   upon   the  state   of  the   peripheral 


Fresiure  5  ozs. 

Fig.   249. — SphygDtographic  tracing  from  a  case  of  Chronic  Brighf  s  disease,  -oith 

hypertrophy  of  the  left  ventricle. 

The  pulse  is  one  of  high  tension  :  the  tidal  wave  is  strongly  marked. 


Flc;.  2^0.  Sphygmographic  tracitig  from  a  case  of  mitral  disease,  after  the 
administration  of  digitalis. 

The  heart  was  much  hypertrophied  ;  the  pulse  was  intermittent,  each  of  the 
pulse  curves  shown  in  the  figure  occupies  the  time  of  two  ordinary  cardiac 
revolutions. 

'  The  special  characters  of  the  pulse  in  aortic  and  mitral  lesions  are  dcbcribed 
on  pages  444,  492,  513,  and  525. 


Hypertrophy  of  tJie  RigJu    Ventricle.  597 

vessels  (whether  firmly  contracted,  atheromatous,  etc.)  ;  the 
tidal  wave  is  usually  very  prominent,  and  the  systolic  portion 
of  the  tracing  more  sustained  than  normal  ;  in  those  cases 
in  which  the  peripheral  vessels  are  not  very  tightly  constricted 
the  up-stroke  is  taller  than  normal.  The  tracings  shown  in 
figs.  249,  250,  and  251,  illustrate  some  of  these  points. 


Pressure  3  '^{^  oz. 

Fig.  251. — Pulse  tracing  ill  a  case  of  hypertrophy  of  the  left  veiifriele  (prohahly\ 
depending  upon  cirrhosis  of  the  kidney. 


HYPERTROPHY   OF   TH?:   RIGHT   VENTRICLE. 

yEtiology. — Hypertrophy  of  the  right  ventricle  is  much  more 
frequently  due  to  extrinsic  than  to  intrinsic  causes,  i.e.  to  con- 
ditions without,  rather  than  within,  the  right  heart. ^  More  or 
less  dilatation  is  almost  always  associated  with  hypertrophy 
of  the  right  heart,  and  in  the  majority  of  cases  the  dilatation 
is  in  excess  of  the  hypcrtroph}'.  In  this  respect,  therefore, 
hypertrophy  of  the  right  ventricle  differs  somewhat  from 
hypertrophy  of  the  left.  Cases  are,  however,  occasionally  met 
with  in  which  the  right  ventricle  is  greatly  hypertrophied,  and 
in  which  there  is  little  or  no  dilatation.  (I  have  before  me 
the  heart  of  a  patient  who  suffered  for  many  years — from 
youth  upwards, — from  chronic  bronchitis  and  emphysema  ;  the 
right  ventricle  is  enormously  hypertrophied,  but  the  cavity  is 
not  dilated.)  Cases  of  this  description  are,  however,  rare,  and 
probably  only  occur  in  young  subjects  in  whom  the  recuper- 
ative powers,  which  favour  the  production  of  hypertrophy,  are 
great,  and  in  whom  the  cardiac  muscle  is  perfectly  healthy. 

'   The  reader  must  remember  that  the  terms  'extrinsic'  and  'intrinsic"  are  here 
applied  not  to  the  heart  as  a  7uho/c,  hut  to  its  right  half  only. 


598  Diseases  of  the   Heart. 

The  conditions  which  produce  hypertroph}-  of  the  right 
ventricle  are  as  follows  : — 

A.  Extrinsic  Causes. 

1.  Mitral  lesions.  (Both  stenosis  and  incompetence.) — 
The  right  ventricle  is  generally  found  (after  deathj  to  be 
considerably  dilated  as  well  as  hypertrophied.  In  the  earlier 
stages  (but  probably  only  in  young  subjects  and  in  cases 
in  which  the  cardiac  muscle  is  not  degenerated),  the  hyper- 
trophy may  for  a  time  be  simple,  i.e.  unattended  by  any 
dilatation. 

2.  Primary  lung  disease. — Emphysema,  cirrhosis,  and  all 
lung  diseases,  which  interfere  with  the  passage  of  the  blood 
from  the  right  to  the  left  heart,  throw  an  increased  strain  on 
the  right  ventricle,  and  tend  to  produce  hypertrophy.  In 
exceptional  cases  the  hypertrophy  is,  as  I  have  just  pointed 
out,  attended  with  little  or  no  dilatation,  i.e.  is  simple;  but  in 
the  large  majority,  dilatation  is  not  only  present,  but  is  in 
excess  of  hypertrophy. 

3.  Narroiuing  of  the  pulmonary  artery  in  eonsequence  oj 
external  pressure. — This  is  an  extremely  rare  cause  of  hyper- 
trophy of  the  right  ventricle,  but  it  does  occasionally  occur. 

B.  Intrinsie  Causes. 
I.  Pulmonary  stenosis. — In  cases  of  congenital  pulmonary 
stenosis,  the  right  ventricle  is  not  always  hypertrophied,  for 
the  foramen  ovale  frequently  remains  patent,  and  by  allowing 
the  blood  to  pass  directly  from  the  right  to  the  left  auricle, 
takes  off  the  strain  from  the  right  heart.  In  those  cases  of 
pulmonary  stenosis,  in  which  the  blood  has  to  pass  through 
the  lungs  in  order  to  get  to  the  left  heart,  the  right  ventricle 
does  become  hypertrophied. 

2.  Pulmonary  incompetenee. — Incompetence  at  the  pulmon- 
ary orifice  is  so  infinitely  rare,  that,  for  practical  purposes,  it 
may  be  left  out  of  account.  It  would  produce  hypertrophy 
and  dilatation  of  the  right  ventricle,  just  as  incompetence  of 
the  aortic  valve  produces  hypertrophy  and  dilatation  of  the 
left. 

3.  Trieuspid  ineompetence. — Primary  tricuspid  incompetence 
is  rare.      It  would  probably  be  attended  by  some  hypertrophy 


Symptoms  of  Hypertrophy  of  t lie  Right  I'cntrictc.    599 

of  the  right  ventricle.  Secondary  tricuspid  incompetence  (the 
result  of  mitral  lesions  or  primary  lung  disease)  occurs  after 
the  right  heart  has  become  dilated,  and  can  hardly,  therefore, 
be  expected  to  produce  much  or  any  hypertrophy  of  the 
right  ventricle.  The  very  fact  that  tricuspid  incompetence  is 
established,  shows  that  the  right  heart  is  failing,  and  unequal 
to  meet  the  demands  upon  it,  i.e.  is  unable  to  become  hyper- 
trophied". 

4.  Pericarditis,  i^'itli  adhesions. — The  effect  of  pericardial 
adhesions  in  producing  hypertrophy  of  the  left  ventricle  has 
already  been  described.  The  same  remarks  apply  to  the 
right  heart,  which  is  probably  more  apt  to  become  hyper- 
trophicd  and  dilated  in  consequence  of  pericardial  adhesions, 
than  the  left. 

Symptoms  and  consequences  of  JiypertropJiy  of  tJie  right 
ventricle. — In  the  great  majority  of  cases,  hypertrophy  of  the 
right  ventricle  is  secondary  to  some  obstruction  in  front.  The 
symptoms  with  which  it  is  associated  are  usually,  therefore, 
those  of  mitral  or  lung  disease,  shortness  of  breath  being  one 
of  the  most  prominent.  The  hypertrophy  itself  is  conserva- 
tive and  salutary.  Hypertrophy  of  the  right  ventricle  may 
be  attended  with  a  feeling  of  tightness,  uneasiness,  beating, 
etc.,  in  the  pit  of  the  epigastrium,  but  sensations  of  this 
description  are  usually  associated  with  dilatation  rather  than 
with  simple  hypertrophy.  The  condition  is  not,  in  fact, 
attended  by  any  characteristic  symptoms.  When  dilatation 
is  combined  with  hypertrophy,  symptoms  of  engorgement  of 
the  .systemic  veins  and  of  embarrassed  pulmonary  circulation 
are  usually  present.^  The  more  the  dilatation  exceeds  the 
hypertrophy  the  greater  will  be  the  venous  engorgement,  the 
greater,  therefore,  the  symptoms,  and  vice  versa. 

The  pulmonary  .symptoms  are  in  part  due  to  the  defective 
blood  supply  to  the  lungs,  which  results  from  the  dilated 
condition  of  the  right  heart,  but  chiefly  to  the  primary  lesion 
— mitral  disease,  or  bronchitis  and  emphysema,  for  example. 

'   .Should   the  tricuspid   give  way,   the  usual  physical   sitjns  of  that   condition 
(systolic  tricuspid  murmur,  jugular  pulsation,  etc.)  will,  of  course,  be  present. 


6oo  Diseases  of  the  Heart. 

Though  hypertrophy  of  the  right  ventricle  is  a  compensatory 
condition  (for  it  enables  the  right  heart  to  cope  with  an 
obstacle  in  front)  it  is  not  an  unmixed  good,  for  the  in- 
creased blood  pressure,  which  is  present  in  the  pulmonary 
circuit  (the  result  partly  of  the  obstruction  in  front  and 
partly  of  the  increased  pressure  from  behind)  is  apt  to 
lead  to  rupture  of  the  pulmonary  capillaries,  and  to  produce 
haemoptysis,  pulmonary  apoplexy,  atheroma  of  the  pulmonary 
artery,  etc. 

The  physieal  signs  of  hypertrophy  of  tlie  right  ventricle  are 
those  of  an  enlarged  and  powerful!}"  acting  right  heart.  The 
left  apex  beat  is,  as  a  rule,  more  diffused  and  displaced  a  little 
to  the  left  (but  not  doivmvards  and  to  the  left  as  it  is  in 
hypertrophy  of  the  left  ventricle),  pulsation  is  often  visible  in 
the  pit  of  the  epigastrium,  or  between  the  left  apex  beat  and 
the  lower  end  of  the  sternum.  On  palpation  the  pulsation  of 
the  right  heart  is  felt  to  be  stronger  than  in  health.  The 
cardiac  dulness  is  increased,  more  especially  in  the  transverse 
direction  and  to  the  right  of  the  sternum.  (See  fig.  252.) 
The  first  sound  o\cr  the  right  ventricle  is,  as  a  rule,  louder 
and  sharper  than  in  health  (hypertrophy  of  the  right  heart  is 
almost  always  associated  \\ith  a  considerable  degree  of  dilata- 
tion) ;  the  second  pulmonar}-  sound  is  accentuated,  and  some- 
times reduplicated.  The  radial  pulse  is,  in  most  cases,  small 
and  weak  (in  consequence  of  the  mitral  lesion  or  lung  disease 
with  which  the  hypertroph}'  of  the  right  ventricle  is  associ- 
ated), and  it  never  presents  the  firm  hard  sustained  character 
which  it  has  in  many  cases  of  hypertrophy  of  the  left  ventricle. 
The  venous  circulation  is  often  congested.  (Congestion  of  the 
systemic  venous  circulation  is  a  sign  of  failure  of  the  right 
heart  rather  than  of  increased  strength,  and  is  indicative  of 
dilatation  rather  than  hypertrophy  ;  it  must,  however,  be  re- 
membered that  some  dilatation  is  almost  always  combined 
with  the  hypertrophy,  and,  as  a  matter  of  fact,  some  venous 
engorgement  is  not  uncommon  in  ca.ses  in  which  signs  of 
hypertrophy  of  the  right  heart  are  well  marked.) 


Hypci'trophy  of  the  Auricles. 


6oi 


Fig.   252. — Hypertrophy  of  the  right  ventricle. — [After  von  Dusch.) 

The  normal   outline  of  the   heart   is   represented    by  a  continuous   line  ;   the 
hypertrophied  right  heart  by  a  dotted  line. 

HYPERTROPHY   OF   THE   AURICLES. 

The  auricles  are  much  more  prone  to  become  dilated  than 
hypertrophied. 


Hypertrophy  of  tJie  Left  Auricle  is  more  frequently   met 
with   than   hypertrophy  of  the  right  ;  it   results    from  mitral 


6o2  Diseases  of  the  Heart. 

stenosis,  and  reaches  its  highest  degree  of  development, 
though  that  is  never  great,  in  young  persons,  and  in  those 
cases  in  which  tlie  cardiac  muscle  is  sound  and  capable  of 
considerable  hy])ertrophy.  Hypertrophy  of  the  left  auricle  is, 
as  we  have  previously  seen,  one  means  by  which  an  obstruc- 
tion at  the  mitral  orifice  is  compensated,  and  is,  therefore, 
beneficial.  It  also  occurs  in  some  cases  of  mitral  regurgita- 
tion. Hypertrophy  of  the  left  auricle  is  not  attended  by  any 
positive  symptoms  or  physical  signs  except  perhaps  the  pre- 
sence of  an  exaggerated  auricular  wave  in  the  cardiographic 
tracing.     (See  fig.  253). 


I'  k;.   253.  —  Caniio'^rapliic  tracing  in  a  case  of  mitral  stenosis. — {After  Galahiii. ) 

'  Henry  A.,  ret  8.  Systolic  and  long,  harsh  presystolic  murmurs  at  the  apex, 
both  accompanied  by  thrill.  The  presystolic  murmur  commenced  immediately 
from  the  second  sound,  and  was  separated  by  a  short  pause  from  the  systole.  The 
bracket  in  the  figure  represents  the  duration  of  the  murmur,  which  is  separated 
by  a  distinct  interval  from  the  ventricular  systole.  The  letter  <?,  indicates  tlic 
gre.itest  auricular  contraction.'' — (Guys  Hospital  Reports,  1875,  P-  3H-) 

Hypertrophy  of  the  left  auricle  may  be  suspected,  when 
the  presence  of  mitral  constriction  is  evidenced  by  a  loud  pre- 
.systolic  murmur,  and  when  the  lung  symptoms,  and  signs  of 
secondary  changes  in  the  right  heart  are  slight.  (The  fact 
that  the  lung  symptoms  and  signs  of  engorgement  of  the  right 
heart  are  slight,  does  not  necessarily  show  that  the  left  auricle 
is  hypertrophied,  for  a  slight  amount  of  mitral  stenosis  will  of 
course  only  produce  slight  engorgement  in  the  pulmonary 
circuit.  A  small  amount  of  constriction  is  not,  as  a  rule, 
attended  by  a  well-marked  presystolic  murmur,  for,  as  we  have 
previously  seen,  a  certain  degree  of  constriction  is  required  for 
the  production  of  the  fluid  vein  on  which  the  murmur  depends. 
If,  therefore,  a  well-marked  presystolic  murmur  is  present,  and 


Hypertrophy  of  tJic  Right  Auricle.  603 

if,  in  addition,  the  symptoms  are  trivial,  and  if  the  signs  of 
secondary  changes  in  the  right  heart  are  shght,  the  probabihty 
is  that  the  lesion  is  not  altogether  a  trivial  one.  Hence  it  is 
allowable  to  conclude,  in  cases  of  this  description,  that  the 
absence  of  lung  symptoms,  and  of  signs  of  right-sided  hyper- 
trophy, are  due  to  compensating  hypertrophy  of  the  left 
auricle.) 

Hypertrophy  of  tiic  Right  Auricle  is  much  more  rare  than 
hypertrophy  of  the  left,  for  tricuspid  stenosis  is,  compared 
with  mitral  stenosis,  a  rare  condition.  The  resisting  power, 
too,  of  the  right  auricle,  is  less  than  that  of  the  left,  and  the 
right  auricle  is,  therefore,  even  more  prone  to  undergo  dilata- 
tion than  the  left.  In  some  cases,  however,  a  considerable 
degree  of  hypertroph}^  is  observed.  The  best  example  which 
has  come  under  my  own  notice  is  the  case  of  primary  lung 
obstruction  (chronic  bronchitis  and  emphysema  from  early 
childhood)  to  which  I  have  previously  referred.  In  that  case 
not  only  was  the  right  ventricle  enormousl}'  hypcrtrophicd 
and  very  little  dilated,  but  the  right  auricle  was  also  notably 
hypertrophied,  and  the  hypertrophy  of  the  right  auricle 
.seemed  in  that  case  to  be  due  to  constriction  of  the  tricuspid 
orifice,  which  in  its  turn  was  apparently  the  result  of  a  thick- 
ening of  the  mu.scular  wall  of  the  heart,  and  twisting  of  the 
tricuspid  segments,  which  were  themselves  health)\  When 
the  right  auricle  is  hypertrophied  as  well  as  dilated,  its  pulsa- 
tions can  usually  be  perceived  in  the  second  and  third  right 
interspaces,  but  to  this  point  I  will  again  refer  under  the  head 
of  dilatation. 

The  Diagnosis  of  Hypertrophy  of  the  Heart. 

The  diagnosis  of  hypertrophy  of  the  ventricles,  more 
especially  of  hypertrophy  of  the  left  ventricle,  is,  as  a  rule, 
easy,  and  is  founded  upon  the  fact  that  the  physical  signs  of 
an  enlarged  and  forcibly  contracting  heart  are  present.  When 
the  lungs  are  emphysematous,  the  diagnosis  may  be  difficult 
or  impossible,  since  it  may  be  impossible  to  discover  either 


6o4  Diseases  of  tJie  Heart. 

the  enlargement  or  the  increased  force  of  the  cardiac  contrac- 
tions. It  must  also  be  remembered  that  enlargement  of  the 
heart,  on  the  one  hand,  may  be  simulated  by  all  those  con- 
ditions in  which  the  pra-cordial  dulness  is  increased  ;  and  that 
the  increased  action  of  a  hypertrophied  heart,  on  the  other, 
may  be  simulated  by  the  forcible  contraction  of  temporary 
(neurotic)  excitement.  Before,  therefore,  diagnosing  hyper- 
trophy of  the  \entricles  (either  right  or  left  or  both),  the 
observer  must  satisfy  himself  that  both  conditions,  viz.  an 
enlarged  and  a  forcibly  contracting  heart  are  present ;  in- 
creased dulness  without  increased  force  of  contraction,  on  the 
one  hand,  and  increased  action  without  increased  dulness  on 
the  other,  being  insufficient.  The  opinion  is,  of  course,  greatly 
strengthened  if  a  distinct  (extra-cardiac  or  intra-cardiac)  cause 
for  the  hypertrophy  is  present. 

The  reader  is  advised  to  refer  to  what  has  been  stated 
with  regard  to  the  differential  diagnosis  of  increased  dulness 
over  the  praecordia,  on  page  129. 

The  differential  diagnosis  of  pericardial  effusion  and  h}'per- 
trophy  of  the  heart  is  given  in  Table  VII.,  page  334;  while 
the  differential  diagnosis  of  hypertrophy  and  dilatation  of  the 
heart  is  discussed  on  page  626. 

The  conditions  which  are  most  likely  to  be  confounded 
with  h\'pcrtrophy  of  the  ventricles  are  : — 

1.  Increased  exposure  of  the  organ,  or  'apparent  enlarge- 
ment^ as  it  may  be  termed. — The  points  to  which  attention  is 
to  be  directed  in  order  to  solve  this  question,  are  detailed  on 
pages  131  and  132,  to  which  the  reader  is  again  referred. 

2.  Temporary  over-action  the  result  of  neurotic  causes 
(neurotic  palpitation). — In  some  cases  the  heart  is,  I  believe, 
actually  enlarged  ;  but,  in  the  majority,  this  is  not  so. 
Cardiac  hypertrophy  is  to  be  excluded  when  the  praecordial 
dulness  is  not  increased,  and  when  the  apex  beat  is  in  its 
usual  position.  The  exact  characters  of  the  pulse  and  of  the 
cardiac  contractions  (whether  slow  and  deliberate,  quick  and 
excited,  etc.),  must  also  be  observed.  In  doubtful  cases  the 
presence    of    any    intra-cardiac    or    extra-cardiac    condition. 


Diagnosis  of  Cardiac  HypertropJiy.  605 

capable  of  producing  hypertrophy,  is  a  fact  of  the  utmost 
importance. 

3.  Displaccuieiit  of  the  heart  dozvmvards  and  to  the  left. — • 
This  condition  may  simulate  hypertrophy  of  the  left  ventricle. 
The  diagnosis  is  to  be  made  by  observing  : — 

{a)  The  force  of  the  cardiac  contractions — increased  in 
hypertrophy,  but  not  increased  in  simple  displacement. 

{U)  The  presence  of  any  cause  of  displacement  (such  as  a 
tumour  or  aneurism  at  the  base  of  the  heart)  on  the  one 
hand,  or  of  hypertrophy  on  the  other  (such  as  cirrhotic 
Bright's  disease,  valvular  lesions,  etc.). 

if)  The  outline  of  the  percussion  dulness — increased  in 
hypertrophy,  simply  altered  in  position,  when  the  heart  is 
displaced. 

TJie  differential  diagnosis  of  hypertrophy  of  the  left  and  rigJit 
ve)itricles  is  not  always  easy  or  possible,  for  the  two  conditions 
are  frequently  combined.  Slight  hypertrophy  of  the  left  ven- 
tricle may  be  masked  by  considerable  hypertrophy  of  the 
right,  and  vice  versa.  In  well  marked  cases  the  distinction  is 
easily  made  by  attention  to  the  following  points  : — 

1.  The  position  of  the  apex  beat  and  cardiac  impulse. — In 
hypertrophy  of  the  left  ventricle,  the  left  apex  beat  is  carried 
downwards  and  outwards,  and  the  area  of  impulse  is  over  the 
left  heart  ;  in  hypertrophy  of  the  right  ventricle,  the  left  apex 
beat  may  be  displaced  somewhat  outwards,  but  not  usually 
downwards,  while  the  area  of  maximum  impulse  is  over  the 
lower  end  of  the  sternum  and  in  the  pit  of  the  epigastrium, 
i.e.  over  the  region  of  the  right  ventricle. 

2.  Tlie  character  of  t/ie  impulse. — In  typical  cases  of  hyper- 
trophy of  the  left  ventricle,  the  apex  beat  is  well  defined  ;  the 
cardiac  impulse  is  deliberate,  forcible,  and  often  has  a  heaving, 
pushing  character.  In  hypertrophy  of  the  right  ventricle,  the 
apex  beat  is,  as  a  rule,  more  diffused  than  in  health  ;  the  im- 
pulse is  not  deliberate,  is  less  forcible  than  in  hypertrophy  of 
the  left  ventricle,  and  does  not  raise  the  chest  wall  en  masse. 

3.  The  outline  of  the  d/dness. — In  h}'pertrophy  of  the  left 
ventricle,  the  increased  cardiac  dulness  extends   both  in  the 


6o6  Diseases  of  the  Heart. 

vertical  and  transverse  directions,  but  chiefly  downwards  and  to 
the  left.  In  hypertrophy  of  the  right  ventricle,  the  increase  in 
the  cardiac  dulness  is  chiefly  transverse,  and  it  extends  to 
the  right  as  well  as  the  left. 

4.  Tlie  character  of  tJie  radial  pulse. — In  h}'pertrophy  of  the 
left  ventricle,  more  particularly  in  those  cases  in  which  the 
h\'pertrophy  depends  upon  extra-cardiac  conditions,  the  radial 
pulse  is  firm  and  strong,  and  has  the  deliberate,  forcible  cha- 
racter possessed  by  the  cardiac  impulse.  In  hypertroph)'  of 
the  right  ventricle  the  radial  pulse  is  usually  small  and  weak. 
When  the  hypertrophy  of  the  left  ventricle  depends  upon 
aortic  or  mitral  valvular  di.sease,  the  firm,  hard,  sustained  pulse 
characteristic  of  hypertrophy  due  to  extra-cardiac  conditions 
(such  as  cirrhotic  Bright's  disease)  is  not  observed.  The  ab- 
sence, therefore,  of  a  hard  sustained  pulse  does  not  exclude 
left-sided  hypertrophy,  but  the  presence  of  a  small  weak  pulse, 
together  with  powerful  pulsation  over  the  right  heart,  is  very 
suggestive  of  right-sided  hypertrophy. 

5.  Tlic  comparative  loudness  of  the  aortic  and  puliiioiiary 
second  sounds. — The  aortic  second  sound  is  accentuated  in 
those  cases  of  hypertrophy  of  the  left  ventricle  which  depend 
upon  extra-cardiac  causes  (when  the  hypertrophy  is  due  to 
mitral  or  aortic  valvular  diseases,  the  accentuation  is  not,  as  a 
rule,  present).  The  pulmonary  second  sound,  on  the  other 
hand,  is  accentuated  when  the  right  ventricle  is  hypertrophied. 
It  must,  however,  be  remembered  that  an  accentuated  pul- 
monary second  sound,  although  highly  suggestive  of  hyper- 
trophy of  the  right  side,  does  not  exclude  hypertrophy  of  the 
left,  for  both  forms  of  hypertrophy  are  often  present  in  the 
same  case,  and  may  in  fact  be  due  to  the  same  primary  cause, 
— viz.  mitral  regurgitation. 

Prognosis. — Hypertrophy  is  a  compensatory  and  beneficial 
condition,  in  fact,  nature's  effort  to  meet  a  difficulty.  It  is 
not,  however,  an  unmixed  good,  since  it  tends  to  produce 
atheroma,  aneurism,  arterial  rupture,  etc. 

The  prognosis  of  cardiac  hypertrophy  depends,  therefore, 
for  the  most  part,  upon   the  cause  of  the  h}'pertroph}\     The 


Treatment  of  Cardiae  Hypertrophy.  607 

form  of  the  hypertrophy  (whether  pure  or  combined  with  dila- 
tation), and  more  especiahy  the  condition  of  the  hypertrophicd 
cardiac  wall  (whether  undergoing  fibroid  or  fatty  changes) 
are  also  important  points.  In  some  cases,  the  cause  of  the 
hypertrophy  can  be  removed,  and  it  then  subsides.  In 
pregnancy  and  acute  Bright's  disease,  for  example,  the 
hypertrophicd  left  ventricle  becomes  quite  normal  with  the 
disappearance  of  its  cause.  The  same  result  also  follows  in 
ca;ses  of  so-called  idiopathic  hypertrophy,  a  condition  which 
is,  I  believe,  present  in  some  cases  of  long  continued  neurotic 
disturbance  of  the  organ. 

In  other  cases — and  these  constitute  the  large  majority — 
the  cause  of  the  hypertrophy  is  permanent.  When  the  pri- 
mary lesion  is  a  stationary  one  {i.e.  non-progressive),  when  the 
hypertrophy  is  pure  {i.e.  unassociated  with  dilatation),  when 
the  cardiac  muscle  is  healthy,  and  when  the  conditions  for 
general  and  local  nutrition  are  satisfactory,  the  prognosis  is, 
on  the  whole,  favourable.  Vice  versa  when  the  lesion  is  pro- 
gressive, when  the  hypertrophy  is  combined  with  dilatation, 
when,  more  especially,  the  cardiac  walls  are  degenerated,  and 
when  the  conditions  for  local  and  general  nutrition  are  unsatis- 
factory, the  prognosis  is  bad.  All  these  points  have,  however, 
been  considered  in  great  detail  under  the  head  of  chronic  val- 
vular lesions,  and  to  that  description  the  reader  is  again 
referred. 

Treatment. — From  what  has  just  been  stated  under  the 
head  of  prognosis,  the  reader  will  perceive  that,  so  long  as  the 
cause  of  the  hypertrophy  remains,  the  hypertrophy  itself  is  to 
be  sustained  and  encouraged,  and  the  nutrition  of  the  heart 
sustained  and  preserved.  It  is  only  in  exceptional  cases,  as, 
for  example,  in  cases  of  idiopathic  hypertrophy,  resulting 
from  neurotic  disturbance,  that  the  hypertrophy  itself  is  to  be 
directly  treated. 

The  indications  for  treatment  in  cases  of  cardiac  hyper- 
trophy are  therefore  : — 

I.  To  remove  its  eaiise. — In  the  majority  of  cases  of  cardiac 
hypertrophy,  the  cause  is  organic  and   permanent,  and   does 


6o8  Diseases  of  tJie  Heart. 

not  permit  of  removal.  In  a  few  cases,  notably,  for  instance, 
in  certain  cases  in  which  high  arterial  tension  depends  upon 
effete  matters  circulating  in  the  blood,  the  excessive  blood 
pressure  can  be  removed,  and  the  hypertrophy,  which  will 
certainly  follow  if  the  high  arterial  tension  continues,  pre- 
vented by  careful  regulation  of  the  diet  and  attention  to  the 
excretions,  more  especially  by  the  administration  of  mercurial 
and  other  purgatives  and  diuretics.  Hypertrophy  due  to  exces- 
sive muscular  effort  and  to  long  continued  neurotic  excite- 
ment of  the  heart  is,  in  many  cases,  curable. 

2.  To  reduce  the  strain  on  tlie  heart  as  much  as  possible. — 
In  those  cases  in  which  the  h}'pcrtrophy  depends  upon 
organic  disease  of  a  permanent  and  incurable  character,  it  is 
important  to  reduce  the  strain  on  the  heart,  and  to  keep  the 
circulation  in  a  tranquil  condition.  The  main  objects  of 
treatment  are — to  avoid  everything  which  is  likely  to  hasten 
the  progress  of  the  lesion  on  which  the  hypertrophy  depends  ; 
and  to  maintain  the  general  state  of  nutrition  and  the  vitality 
of  the  cardiac  muscle,  so  as  to  enable  it  to  meet  the  extra 
demand  which  is  required  of  it,  and  to  compensate  the  lesion. 
In  short,  the  whole  object  of  treatment  is  to  keep  the  primary 
lesion  in  a  stationary  or  static  condition,  and  to  maintain  just 
so  much  hypertrophy  as  is  sufficient  to  balance  the  defect. . 
In  cases  of  this  description  it  is  particularly  important  to 
avoid  all  sudden  causes  of  cardiac  strain  and  excitement ;  in 
hypertrophy  of  the  right  ventricle,  for  example,  whether  the 
hypertrophy  results  from  a  mitral  lesion  or  from  a  primary 
lung  disease,  acute  pulmonary  complications,  such  as  attacks 
of  bronchitis,  which  necessarily  throw  an  increased  and 
sudden  strain  on  the  right  heart,  must  be  carefully  guarded 
against.  Many  other  instances  of  a  similar  kind  might  of 
course  be  mentioned,  and  many  other  details  of  treatment 
given,  but  the  subject  has  been  so  fully  considered  under 
the  head  of  cardiac  valvular  lesions,  that  I  must  content 
myself  with  referring  the  reader  to  the  previous  portions  of 
this  work. 

When  any  indications  of  cardiac  failure  arise,  the  adminis- 
tration of  digitalis  and  other  cardiac  tonics  and  stimulants  is 


Dilatation  of  the  Heart.  609 

called  for.  In  fact,  the  treatment  which  is  appropriate 
for  the  early  stages  of  dilatation  of  the  heart,  must  then  be 
carried  out. 

The  occurrence  of  palpitation  in  cases  of  hypertrophy  is 
usually,  as  I  have  previously  insisted  upon,  an  indication  of 
commencing  failure  and  of  cardiac  embarrassment.  It  is  to 
be  treated  by  reducing  the  strain  on  the  heart,  and  by  the 
administration  of  cardiac  tonics,  more  especially  digitalis. 
When  the  palpitation  is  due  to  neurotic  causes,  i.e.  when  it  is 
not  indicative  of  cardiac  failure,  cardiac  seditives  are  indi- 
cated. The  application  of  cold,  in  the  form  of  ice-bags,  to 
the  region  of  the  heart ;  and  the  internal  administration  of 
aconite  (drop  doses  every  hour,  carefully  watched),  of  vera- 
trum  viride  (five  drops  of  the  tincture  three  times  daily),  of 
digitalis  and  of  hydrocyanic  acid  (two  minim  doses  every 
three  or  four  hours),  are  the  most  useful  remedies.  The 
application  of  a  belladonna  plaster  to  the  praecordia  also 
seems  in  some  cases  to  be  beneficial. 

DILATATION   OF   THE   HEART. 
Definition. — Increased  size  of  the  cardiac  cavities. 

Varieties. — Three  varieties  of  dilatation  are  usually  de- 
scribed, viz. : — 

I.  Simple  dilatation. — In  this  form  the  cardiac  cavities  or 
cavity — for  one  cavity  only  may  be  affected — are  enlarged, 
and  the  muscular  wall  of  the  cavity  retains  its  normal  thick- 
ness. The  total  amount  of  muscular  tissue  surrounding  the 
dilated  cavity  is  necessarily  increased,  for  otherwise  it  would 
be  impossible  for  the  wall  of  the  cavity,  the  area  of  which  is 
increased,  to  retain  its  normal  thickness.  Simple  dilatation  of 
the  heart  is  therefore  impossible,  provided  that  the  wall  of  the 
dilated  cavity  remains  healthy  ;  but  since,  in  many  cases,  the 
muscular  tissue  is  replaced  by  fibroid  tissue,  simple  dilatation 
is  possible,  if  we  regard  the  amount  of  muscular  tissue  tn  the 
cardiac  zuall,  and  not  the  mere  thickness  of  the  wall  itself 
The  distinction  may  perhaps  seem  a  fine  one,  but  it  is  not 
without  practical  advantages,  for  the  muscular  tissue  of  the 

Q  Q 


6io  Diseases  of  t lie  Heart. 

wall  is  the  important  clement ;  and  it  is  essential  in  looking 
at  the  wall  of  a  dilated  heart,  just  as  it  is  in  looking  at  the 
wall  of  an  apparently  hypertrophied  heart,  to  endeavour  to 
determine  whether  it  is  composed  of  healthy  muscular  fibre 
or  not. 

2.  Dilatation  witJi  Hypertrophy} — This  condition,  which 
used  to  be  called  active  dilatation,  is  by  far  the  most  common 
form,  so  far,  at  all  events,  as  the  ventricles  are  concerned. 
The  relative  proportions  of  dilatation  and  hypertrophy  vary 
indefinitely  in  different  cases.  When  the  hypertrophy  is  in 
excess  or  considerable,  the  condition  is  synonymous  with 
eccentric  hypertrophy  ;  when  dilatation  exceeds  hypertrophy, 
the  term  dilatation,  without  any  qualification,  or  dilatation 
with  JiypertropJiy,  is  generally  applied. 

3.  Dilatation,  ivith  thinning  or  passive  dilatation,  as  it  is 
sometimes  termed. — This  form  is  not  so  common  as  the  pre- 
ceding ones,  but  it  is  occasionally  seen  in  the  auricles,  more 
especially  the  right  auricle.  As  the  term  indicates,  the  cavity 
is  dilated,  and  the  wall  thinner  than  natural.  Cases  of  dilata- 
tion with  thinning  of  the  muscular  tissue  of  the  wall  (if  we 
regard  the  muscular  fibres  alone,  irrespective  of  the  endocar- 
dium, pericardium,  and  fibroid  tissue  and  fat),  are  probably 
more  common  than  is  generally  supposed. 

Etiology  a Jid  Pathology.— \]ndcr  normal  circumstances  the 
walls  of  the  different  cardiac  cavities  possess  sufficient  resist- 
ing power  to  withstand  the  pressure  of  the  blood  which  they 
contain.  When,  however,  the  cardiac  wall  is  weakened  by 
disease,  or  when  the  blood  pressure  within  the  cavity  is  in- 
creased to  such  an  extent  that  the  existing  power  of  the  wall 
of  the  cavity  is  overcome,  yielding  or  dilatation  of  the  cavity 
will  result.  The  great  causes  of  cardiac  dilatation  are  there- 
fore in  some  cases  vital,  in  others  mechanical,  viz. : — 

'  Under  the  head  of  dilatation  with  hypertrophy,  those  cases  of  so-called 
simple  dilatation  {i.e.  dilatation  with  normal  thickness  of  wall)  in  which  the  wall  of 
the  dilated  cavity  is  composed  of  muscular  tissue,  ought,  strictly  speaking,  to  be 
included  ;  for,  in  cases  of  this  description,  the  total  amount  of  muscular  tissue  in 
the  wall  of  the  affected  cavitv  is  increased. 


Aitiology  and  Patholooy  of  Cardiac  Dilatation.  6 1 1 

I.  Diminished  resisting  pozver  of  the  cradiac  zvalts. — All 
conditions,  which  impair  the  vitality  and  integrity  of  the  mus- 
cular tissue,  impair,  of  course,  the  resisting  power  of  the 
cardiac  wall.  In  some  cases,  the  structural  change  in  the 
cardiac  muscle  is  quickly  established,  i.e.  is  acute  ;  under  this 
head  are  included  acute  fatty  degeneration,  acute  myocarditis, 
acute  ulcerative  endocarditis,  and  the  muscular  changes  (cloudy 
swelling  and  softening)  which  are  met  with  in  the  continued 
fevers.  In  other  cases,  the  muscular  lesion  is  slowly  estab- 
lished ;  in  this  group  are  included  fatty  infiltration,  fatty 
degeneration,  fibroid  degeneration,  the  relaxed  and  debilitated 
condition  of  the  cardiac  muscle,  which  is  associated  with 
anaemia,  impaired  general  nutrition,  conditions  of  nervous 
depression  and  general  muscular  relaxation.  The  conditions, 
therefore,  which  produce  the  structural  changes  in  the  cardiac 
wall  leading  to  diminished  resistance,  and  therefore  to  dilata- 
tion, are  in  some  cases  local  and  in  others  general ;  the  fibroid 
degeneration  which  results  from  myocarditis,  is  an  example 
of  the  former  ;  the  fatty  degeneration,  associated  with  general 
anaemia  (chlorosis  and  progressive  pernicious  anaemia)  of  the 
latter. 

When  the  resisting  power  of  the  cardiac  wall  is  much  im- 
paired, dilatation  may  result  under  the  normal  blood  pressure. 
When  the  lesion  of  the  muscle  is  a  slight  one,  an  abnormal  de- 
gree of  blood  pressure  may  be  required  to  produce  dilatation ; 
and,  as  a  matter  of  fact,  both  causes  are  frequently  combined. 
The  lesion,  which  produces  the  diminished  resistance,  may  be 
limited  to  a  particular  part  of  the  wall  of  one  cardiac  cavity 
— the  left  ventricle,  for  example — the  dilatation  which  results 
will,  of  course,  be  local,  and  the  condition  is  then  synonymous 
with  that  which  has  been  previously  described  under  the  term 
aneurism  (partial  or  local  aneurism)  of  the  heart.  In  other 
cases,  the  whole  wall  of  one  cavity  is  affected,  and  the  whole 
of  that  cavity  becomes  dilated ;  to  these  cases  the  term 
partial  dilatation  of  the  heart  is  sometimes  applied.^     In  others 

•  Partial  dilatation  of  the  heart  must  not  be  confounded  with  partial  or  local 
dilatation  oi  one  cavity,  i.e.  with  the  condition  which  is  more  appropriately  termed 
aneurism  of  the  heart. 


6 1 2  Diseases  of  the  Heart. 

again  the  dilatation  affects  all  the  cavities  of  the  heart ;  it  is 
then  said  to  be  general. 

2.  Increased  blood  pressure  within  the  heart. — Increased 
blood  pressure  is,  of  course,  a  mechanical  cause  of  dilatation  ; 
and  other  things  being  equal,  the  greater  the  pressure  the 
greater  the  dilatation.  It  must  not,  however,  be  supposed 
that  the  problem  is  entirely  a  mechanical  one.  Several  im- 
portant considerations,  more  especially  the  rapidity  with  which 
the  increased  pressure  is  established,  the  vitality  of  the  cardiac 
muscle,  the  reserve  force  possessed  by  the  wall  of  the  particu- 
lar cavity  on  which  the  increased  pressure  is  exercised,  and 
the  condition  of  the  cardiac  wall  (whether  relaxed  or  con- 
tracted) at  the  time  when  the  pressure  is  applied,  all  exert  an 
important  influence  on  the  result. 

(a)  The  rapidity  ivith  ivhich  the  pressure  is  established 
and  the  vital  condition  of  the  cardiac  muscle. — When  the 
increased  pressure  is  quickly  established,  and  when  that 
pressure  is  in  excess  of  the  resisting  power  {i.e.  of  the 
reserve  force)  possessed  by  the  cardiac  wall  on  which  it  is 
brought  to  bear,  dilatation  must  necessarily  result. — I  do  not, 
of  course,  refer  to  those  cases  in  which  the  excessive  pressure 
is  so  great  as  to  produce  paralysis  of  the  cardiac  wall,  in 
such  cases  death  would  of  course  result ;  nor  to  those  cases  in 
which  the  pressure  is  of  merely  temporary  duration,  tem- 
porary over-distention  of  the  right  heart  is  of  frequent  occur- 
rence, and  is  probably  relieved  by  the  yielding  (safety-valve 
action)  of  the  tricuspid  valve,  which  may,  of  course,  occur 
even  when  the  muscular  tissue  of  the  cardiac  wall  is  perfectly 
healthy.  One  of  the  best  examples  of  dilatation  produced  in 
this  manner  is  that  which  follows  the  sudden  rupture  of  an 
aortic  valve  segment. 

But  even  in  cases  of  this  description  the  dilatation  is 
not  pure  {i.e.  unattended  with  hypertrophy),  for  although 
the  dilatation  always  remains  in  excess — and  usually  largely 
in  excess — a  certain  amount  of  hypertrophy  is  gradually 
established.  Provided  that  the  cardiac  muscle  is  sound,  it 
is  almost  impossible  to  have  pure  dilatation.  Should  the 
patient  survive  a  sufficient  length  of  time,  some  increase  of 


Aitiology  and  Pathology  of  Cardiac  Dilatation.  6 1 3 

the  muscular  wall,  i.e.  some  hypertrophy,  will  almost  certainly 
occur ;  the  dilated  cavity  contains  an  excessive  quantity  of 
blood,  its  muscular  wall  is  consequently  over-stimulated,  and, 
provided  that  its  muscular  fibre  is  healthy,  the  increased  strain 
which  is  thrown  upon  it,  and  the  excessive  efibrt  which  is  put 
forth  in  its  attempts  to  expel  the  abnormally  large  quantity 
of  blood  which  it  contains,  will  almost  of  necessity  result  in 
the  production  of  some  hypertrophy.  When,  therefore,  the 
blood  pressure  within  the  heart  is  quickly  raised  beyond  the 
resisting  power  of  the  cardiac  wall,  dilatation  is  necessarily 
produced,  but  the  walls  of  the  dilated  cavity  tend  at  the 
same  time  to  become  hypertrophied.  As  a  matter  of  fact, 
however,  the  dilatation  almost  invariably  remains  in  excess, 
and,  as  a  rule,  largely,  in  excess  of  the  hypertrophy. 

When,  on  the  other  hand,  the  increased  pressure  is  very 
slowly  and  gradually  established,  hypertrophy  results,  pro- 
vided, of  course,  as  has  been  previously  explained,  that  the 
vitality  of  the  cardiac  muscle  is  good  and  it  is  able  to  respond 
to  the  increased  strain  which  is  thrown  upon  it.  In  cases  of 
this  description,  the  pressure  is  in  fact  never  in  excess  of  the 
reserve  force,  for,  as  the  pressure  slowly  and  gradually  in- 
creases, the  resisting  power  keeps  pace  with  it,  in  consequence 
of  the  hypertrophy,  which  is  pari pass2i  established.  The  hy- 
pertrophy of  the  left  ventricle,  which  accompanies  the  cirrhotic 
form  of  Bright's  disease,  is  a  typical  example  in  point. 

When,  however,  the  cardiac  walls  are  degenerated,  increased 
pressure  produces  dilatation,  however  slowly  and  gradually  it 
is  established.  And  even  in  those  cases  in  which  the  muscular 
fibre  was  originally  sound  and  the  hypertrophy  for  a  time 
pure,  dilatation  often  ultimately  follows  in  consequence  of 
degenerative  changes,  which  are  so  apt  to  occur  in  the  walls  of 
a  hypertrophied  heart. 

We  may  say,  then,  that  a  dilated  heart,  whose  muscular 
walls  are  healthy,  tends  to  become  hypertrophied,  while  a 
hypertrophied  heart  tends  ultimately  to  become  dilated. 

(b)  The  cavity  on  zvhich  the  increased  pressure  is  exerted. — 
The  weaker  the  wall  the  greater  the  tendency  to  dilatation  ; 
hence  it  is  that  the  auricles,  the  walls  of  which  possess  little 


6 14  Diseases  of  the  Heart. 

reserve  force,  are  more  liable,  other  things  being  equal,  to 
become  dilated  than  the  ventricles,  and  the  cavities  of  the 
right  heart  than  those  of  the  left.  The  order  then  in  which 
the  cardiac  cavities  tend  to  become  dilated  is  as  follows  : — 

Right  auricle. 

Left  auricle. 

Right  ventricle. 

Left  ventricle. 
The  clinical  and  pathological  conditions,  which  produce 
increased  pressure  within  the  cardiac  cavities,  and  which  may 
therefore  lead  to  dilatation,  are  very  various.  The  more  im- 
portant have  been  mentioned  in  speaking  of  the  causes  of 
hypertrophy.  Increased  tension  in  the  left  ventricle,  during 
its  systole,  is  produced  by  all  those  conditions  which  interfere 
with  the  passage  of  the  blood  through  the  arterial  and  capil- 
lary systems,  or  which  cause  obstruction  at  the  aortic  orifice. 
(These  conditions  are,  as  we  have  previously  seen,  more  likely 
to  produce  hypertrophy  than  dilatation.)  Aortic  incompe- 
tence and  mitral  incompetence  produce  over-distention  of 
the  left  ventricle  during  its  diastole,  and  are  fertile  sources  of 
dilatation  of  that  cavity. 

Mitral  stenosis  and  mitral  incompetence  both  produce 
increased  tension  in  the  left  auricle  (the  former  during  sys- 
tole, the  latter  during  diastole),  and  both  cause  dilatation  of 
that  cavity.  Aortic  lesions  and  increased  tension  in  the 
arterial  system  may  ultimately  lead  to  the  same  result. 

Over-distention  of  the  right  ventricle,  during  its  systole,  is 
produced  by  all  conditions  which  interfere  with  the  blood- 
flow  through  the  lungs  (primary  lung  disease,  mitral  lesions, 
etc.),  or  which  cause  an  obstruction  at  the  pulmonary  orifice 
or  in  the  pulmonary  artery.  Tricuspid  incompetence  pro- 
duces over-distention  of  the  right  ventricle  during  its  diastole. 
All  of  these  conditions  cause  dilatation.  (Pulmonary  incom- 
petence is  so  extremely  rare,  that  for  practical  purposes  it  may 
be  left  out  of  account.)  Increased  tension  of  the  blood  in  the 
right  auricle  is  usually  due  to  some  obstruction  in  front  of  the 
right  ventricle,  or  to  tricuspid  incompetence,  or  to  both  con- 
ditions combined.     Tricuspid  stenosis  of  course  produces  the 


yEtiology  and  Pathology  of  Cardiac  Dilatation.  6 1 5 

same  result,  i.e.  over-distention  and  dilatation  of  the  right 
auricle. 

(c)  T/ic  condition  of  the  cardiac  zvatt  {w/ietlier  flaccid  or 
contracted)  at  the  time  zvJien  tJie  pressure  is  exercised. — Forcible 
dilatation  of  the  cardiac  wall  when  it  is  in  a  flaccid  and 
enlarged  condition,  i.e.  during  its  diastole,  is  much  more  likely 
to  produce  dilatation  than  forcible  pressure  when  the  wall  is 
contracted,  i.e.  during  the  systole.  (This  statement  does  not, 
however,  apply  to  those  cases  in  which  a  limited  portion  of 
the  cardiac  wall  has  lost  its  resisting  power,  in  consequence  of 
degenerative  changes.)  It  is  probably  in  consequence  of  this 
fact  that  the  cavity  of  the  left  ventricle  becomes  dilated  in 
aortic  and  in  mitral  incompetence.  In  the  former  case,  i.e. 
aortic  regurgitation,  blood  is  poured  into  the  cavity  from  two 
sources,  viz.  from  the  left  auricle  through  the  mitral  in  the 
normal,  and  from  the  aorta  in  the  reverse  course  of  the  circula- 
tion ;  the  left  ventricle  becomes  more  quickly  and  more  forcibly 
distended  than  in  health,  and  before  the  occurrence  of  each 
systole  it  is,  as  it  were,  dilated.  In  the  latter  case,  i.e.  mitral 
incompetence,  the  blood  stream,  which  passes  through  the 
mitral  orifice  is  a  larger  and  more  forcible  stream  than  in 
health,  in  consequence  of  the  excessive  blood  pressure  in  the 
parts  behind  the  affected  {i.e.  mitral)  orifice. 

During  their  systole,  on  the  other  hand,  the  walls  of  the 
heart  are  able  to  withstand  high  internal  pressure  without  the 
production  of  dilatation.  The  pressure  within  the  left  ven- 
tricle, for  example,  during  the  systole  of  a  normal  heart,  is 
extremely  great ;  it  is  still  greater  in  cases  of  aortic  stenosis 
in  which  the  blood-flow  from  the  cavity  is  obstructed  and  the 
wall  of  the  cavity  hypertrophied  ;  and  yet  the  hypertrophy 
is  in  many  cases  pure,  i.e.  unattended  with  any  dilatation. 
When,  therefore,  the  increased  pressure  is  brought  to  bear 
during  systole,  the  tendency  to  dilatation  is  comparatively 
slight.  But  since  these  points  have  been  fully  explained, 
when  treating  of  the  different  valvular  lesions,  I  must  refer 
the  reader  to  what  has  been  already  said  on  those  subjects 
for  further  details.  In  cases  of  this  nature  local  dilatations 
or  partial  aneurisms  of  the  heart  are,  as  we  have  previously 


6i6  Diseases  of  the  Heart. 

seen,  produced,  the  weakened  part  of  the  cardiac  wall  yield- 
ing to  the  very  great  internal  pressure  produced  during  the 
cardiac  systole. 

3.  Traction  from  without. — Theoretically  this  is  a  possible 
cause  of  cardiac  dilatation  ;  and,  as  a  matter  of  fact,  we  find 
that  in  many  cases  of  adherent  pericardium  cardiac  dilatation  is 
actually  present.  In  some  of  these  cases  the  dilatation  is 
undoubtedly  due  to  other  conditions  (more  especially  associ- 
ated valvular  lesions)  and  not  to  the  adherent  pericardium  ; 
in  other  cases  in  which  the  cardiac  valves  are  healthy,  but  the 
pericardium  adherent,  the  dilatation  is  chiefly  due  to  structural 
changes  in  the  cardiac  muscle  which  are  so  frequently  present  ; 
traction  from  without  is  probably,  in  part  at  least,  the  cause  of 
the  dilatation  in  some  cases  of  adherent  pericardium.  When, 
on  the  contrary,  the  muscular  walls  are  healthy,  pericardial 
adhesions,  by  the  resistance  which  they  offer  to  the  free  con- 
traction of  the  organ,  are  apt  to  produce  hypertrophy.  In 
short,  the  result  (whether  hypertrophy  or  dilatation)  which 
is  produced  by  pericardial  adhesions  depends,  in  my  opinion, 
chiefly  upon  the  vitality,  so  to  speak,  of  the  cardiac  wall,  and 
upon  the  part  of  the  heart  upon  which  the  traction  is  exer- 
cised. When  the  cardiac  wall  is  healthy,  hypertrophy  will 
probably  result.  When,  on  the  contrary,  the  cardiac  wall  is 
degenerated,  dilatation  will  probably  be  produced  (other 
things  being  equal).  Traction  on  the  wall  of  the  right  ven- 
tricle is  more  likely  to  produce  dilatation  than  traction  on 
the  wall  of  the  left,  for  the  reserve  force,  and  therefore  the 
tendency  to  hypertrophy,  is  greater  in  the  left  ventricle  than 
in  the  right. 

Both  results  (hypertrophy  and  dilatation)  are  more  likely 
to  occur  when  the  pericardial  sac  is  adherent  to  the  parts 
external  to  it  (sternum,  lungs,  etc.),  as  well  as  to  the  surface 
of  the  heart.  The  more  extensive  the  adhesions  the  greater  the 
tendency  both  to  hypertrophy  and  to  dilatation. 

Dilatation  is  said  to  occur  sometimes  in  health  as  the 
result  of  violent  muscular  efforts  or  other  sudden  causes  of 
cardiac  over-distention  ;  but  whether  such  a  result  does  ever 
occur  in  perfect  health  is,  in  my  opinion,  extremely  doubtful. 


yEtiology  and  PatJiology  of  Cardiac  Dilatation.  6 1 7 

Doubtless  over-distcntion,  of  the  right  heart  more  particularly, 
is  of  frequent  occurrence,  and  it  may  be  granted  that  if  such 
over-distention  were  frequently  repeated,  some  permanent  di- 
latation would  probably  remain.  Occasional  over-distention 
could  hardly,  I  think,  lead  to  permanent  dilatation  unless  the 
resisting  power  of  the  cardiac  muscle  were  lowered,  in  con- 
sequence of  some  general  constitutional  cause  or  local  struc- 
tural defect. 

The  naked  eye  appearances  which  a  dilated  heart  presents 
(its  size  and  weight,  shape,  etc.)  vary  of  course  with : — the 
part  of  the  organ  which  happens  to  be  affected,  the  extent  of 
the  dilatation,  the  condition  of  the  pericardium,  the  amount 
of  sub-pericardial  fat,  and  the  state  of  the  cardiac  muscle, 
whether  flaccid,  as  the  result  of  fatty  or  other  changes,  or 
indurated  as  the  result  of  combined  hypertrophy  and  fibroid 
degeneration.  It  is  unnecessary  to  go  into  details.  The  micro- 
scopical appearances,  too,  are  very  varied.  In  some  cases  the 
muscle  is  fairly  healthy  ;  in  others,  fatty  and  fibroid  changesi 
are  present ;  in  others,  again,  cloudy  swelling,  or  acute  myo- 
carditis is  observed.  All  of  these  conditions  are  described  in 
detail  in  other  parts  of  the  work,  and  need  not  be  repeated. 

Pathological  Physiology. — Dilatation,  which  is  the  direct 
opposite  of  hypertrophy,  inasmuch  as  it  impairs  the  efficiency 
of  the  cardiac  pump,  is  an  injurious  condition.  But  while  this 
statement  may  be  safely  laid  down  as  a  general  proposition, 
there  are  some  circumstances  in  which  a  certain  degree  of 
dilatation  is  beneficial  and  compensatory.  In  regurgitant  val- 
vular lesions  (say  mitral  regurgitation,  for  example)  dilatation 
of  the  cavity  which  is  situated  behind  the  affected  orifice  (i.e. 
the  left  auricle  in  the  case  we  are  considering)  is  beneficial, 
provided  that  it  is  just  sufficient  to  accommodate  the  blood 
which  regurgitates  at  each  systole,  and  provided  that  the  wall 
of  the  dilated  cavity  {i.e.  of  the  left  auricle)  is  at  the  same 
time  sufficiently  hypertrophied  to  completely  empty  the 
cavity,  i.e.  to  expel  into  the  cavity  of  the  left  ventricle  all  the 
blood  which  has  regurgitated, togetherwith  the  normal  quantity 
of  blood  which  reaches  it  from  the  pulmonary  veins.     Such  a 


6i8  Diseases  of  tJie  Heart. 

perfect  balance  of  compensation  is,  however,  rarely  seen  ; 
and,  speaking  generally,  it  may  be  safely  affirmed  that  dilata- 
tion is  a  baneful  condition  ;  blood  tends  to  stagnate  in  the 
dilated  cavity,  the  circulation  in  the  parts  behind  becomes 
retarded,  the  supply  of  blood  to  the  parts  beyond,  defective  ; 
in  short,  a  condition  of  arterial  anaemia  and  venous  engorge- 
ment, with  all  the  secondary  results  and  complications,  which 
I  have  fully  described  in  speaking  of  mitral  and  tricuspid 
valvular  lesions,  tends  to  become  established.  When  the 
dilated  cavity  is  a  ventricle,  relative  incompetence  of  the 
auriculo-ventricular  valve  connected  with  it  is  also  apt  to  be 
produced.  Dilatation  of  the  left  ventricle  is  apt  to  produce 
incompetence  of  the  mitral,  and  dilatation  of  the  right  ven- 
tricle of  the  tricuspid  orifice.  Clots  are  apt  to  form  in  those 
parts  of  the  cardiac  cavities  in  which  the  blood  current  is 
sluggish  or  stagnant  (the  appendices  of  the  auricles,  apices  of 
the  ventricles,  etc.)  Portions  of  these  clots  may  become 
detached  and  carried  as  embolic  infarctions  to  distant  parts. 
In  rarer  cases,  alarming  symptoms  and  death  result  from  the 
presence  of  thrombi  within  the  heart  itself  To  sum  up,  in 
dilatation  a  greater  amount  of  blood  requires  expulsion  from 
the  dilated  cavity  ;  the  walls  of  the  cavity  have  less  power 
than  normal ;  in  addition,  valvular  incompetence  (mitral  and 
tricuspid  regurgitation)  is  often  established  ;  clots  may  form 
in  the  dilated  cavity,  and  embolic  plugging  of  distant  vessels 
may  be  produced. 

Symptoms. — The  symptoms  which  characterise  dilatation 
of  the  heart  are  essentially  those  of  cardiac  weakness,  engorge- 
ment of  the  venous,  and  anaemia  of  the  arterial,  circulations. 
Differences  in  detail  are,  of  course,  observed  in  accordance 
more  particularly  with  the  seat  of  the  lesion  {i.e.  whether  the 
left  or  the  right  heart  is  affected),  the  extent  of  the  dilatation, 
and  the  associated  pathological  conditions  (degree  of  hyper- 
trophy which  accompanies  the  dilatation,  the  presence  of  as- 
sociated valvular  lesions). 

In  advanced  cases  of  dilatation  of  the  left  heart,  the  symp- 
toms are  identical  with  those  of  advanced  mitral  lesions.     (See 


Physical  Signs  of  Cardiac  Dilatation.  6 1 9 

page  439.)  In  advanced  dilatation  of  the  right  heart,  the 
symptoms  correspond  to  those  of  tricuspid  regurgitation.  (See 
page  534-) 

Physical  signs. — The  physical  signs  which  are  met  with  in 
dilatation  of  the  heart  vary,  of  course,  with  the  nature  of  the 
primary  lesion  on  which  the  dilatation  depends,  and  the  parti- 
cular part  of  the  organ  which  is  dilated.  The  physical  signs 
characteristic  of  dilatation  per  se  {i.e.  irrespective  of  the  pri- 
mary lesion  on  which  the  dilatation  depends),  are  indicative  of 
enlargement  and  weakness  of  the  heart.  Here,  as  in  the  case 
of  hypertrophy,  it  is  essential  to  remember  that  the  physical 
signs  indicative  of  the  size  of  the  heart  and  the  strength  of 
the  cardiac  impulse,  are  materially  modified  by  the  condition 
of  the  lungs.  When  the  lungs  are  emphysematous,  it  may  be 
difficult  or  impossible  to  detect,  by  means  of  percussion,  en- 
largement of  the  organ.  (This  statement  applies  more  espe- 
cially to  enlargement  of  the  left  side.)  When,  again,  the  lungs 
are  very  voluminous,  the  force  of  the  cardiac  impulse  as  felt  by 
the  hand  over  the  prjecordia,  is  diminished,  and  the  conduction 
of  the  cardiac  sounds  to  the  ear  interfered  with  ;  under  such 
circumstances  the  heart  may  be  acting  with  quite  the  normal 
strength,  but  may  appear  to  be  weak.  An  emphysematous 
condition  of  the  lungs  adds,  therefore,  considerably  to  the 
difficulties  of  diagnosing  a  dilated  heart ;  for,  on  the  one  hand, 
it  may  be  difficult  or  impossible,  when  the  heart  is  actually 
dilated,  to  detect  the  enlargement  by  means  of  percussion,  and, 
on  the  other,  a  perfectly  normal  or  even  hypertrophied  heart 
may  appear  (owing  to  the  feeble  impulse  and  feeble  sounds) 
to  be  weak. 

In  conditions  of  general  dilatation,  the  impulse  both  of  the 
left  and  right  hearts  is  weaker  than  in  health  ;  the  apex  beat 
is  feeble,  or  altogether  imperceptible.  When  the  right  ventricle 
is  dilated  and  the  left  normal,  the  impulse  over  the  right  heart 
is  feeble  or  imperceptible  ;  the  impulse  of  the  left  heart  may 
be  of  normal  strength.  It  must,  however,  be  remembered  that 
when  the  right  ventricle  is  dilated,  it  may  be  difficult  or  im- 
possible to  distinguish  the  impulse  of  the  left  heart,  for  the 


620  Diseases  of  the  Hearf. 

heart  is  rotated  on  itself,  the  right  ventricle  making  its  way  in 
front  of  the  left.  The  impulse,  when  it  can  be  felt,  is  usually 
more  diffused  than  in  health,  and  consists  of  a  short  slap  or  tap, 
indicative  of  a  quick,  short,  irritable  and  feeble  ventricular 
contraction,  the  exact  opposite  of  the  prolonged,  steady,  deli- 
berate heave  of  hypertrophy.  The  cardiac  action  is  often 
irregular  ;  and  the  frequency  of  the  cardiac  contractions  is  ver>' 
generally  increased. 

The  position  of  the  apex  beat  varies  in  accordance  with 
the  part  of  the  heart  which  is  dilated.  In  dilatation  of  the 
left  ventricle,  the  left  apex  beat  can  usually  be  felt  (for  the 
dilatation  is  generally  combined  with  some,  often  with  con- 
siderable, hypertrophy),  and  is  displaced  downwards  and  to 
the  left ;  when  the  right  ventricle  is  dilated,  the  left  apex  beat 
is  often  effaced,  owing  to  the  fact  that  the  right  ventricle 
makes  its  way  in  front,  displacing  the  left  heart  backwards 
and  to  the  left ;  when  the  right  heart  is  much  dilated,  pulsation 
can  often  be  seen  and  felt  in  the  second  left  interspace.  In 
some  cases  this  pulsation  is,  I  think,  derived  from  the  conus 
arteriosus  of  the  right  heart ;  in  others,  from  a  dilated  pulmon- 
ary artery.  When  the  left  auricle  is  very  much  dilated,  as  it  is 
in  some  cases  of  mitral  stenosis,  for  example,  its  pulsation  can 
sometimes,  it  is  said,  be  seen  and  felt  in  the  second  left  inter- 
space. I  am  not  prepared  to  say  unconditionally  that  this 
auricular  pulsation  does  not  occur,  but  I  have  never  seen  any 
post-7)iortem  evidence  in  support  of  it.  When  the  right  auricle 
is  much  dilated,  pulsation  sometimes  can  be  felt  in  the  third 
right  interspace  adjacent  to  the  sternum.  When  the  tricuspid 
is  incompetent,  as  it  very  generally  is  in  cases  of  this  descrip- 
tion, the  pulsation  is  systolic  in  rhythm,  and  accompanied  by 
true  venous  pulsation  in  the  neck  and  often  also  in  the  liver. 

The  area  of  percussion  dulness  (both  superficial  and  deep) 
is  increased  (except  as  previously  mentioned  in  conditions  of 
emphysema)  ;  the  direction  of  the  increase  varies  in  accordance 
with  the  particular  part  of  the  heart  which  is  dilated.  (See 
figs,  246  and  252.)  When  the  left  ventricle  is  affected,  the 
increased  dulness  extends  both  in  the  vertical  and  transverse 
directions,  and  is  chiefly  downwards  and  to  the    left ;  when 


Physical  Signs  of  Cardiac  Dilatation.  62 1 

the  right  ventricle  is  dilated,  the  increased  dulness  is  for  the 
most  part  transverse. 

When  the  ventricles  are  dilated,  the  duration  of  the  first 
sound  is  shorter  than  in  health,  its  pitch  higher  ;  it  is  in  fact 
more  valvular  and  less  muscular  than  the  normal  first  sound  ; 
in  many  cases  it  is  with  difficulty  distinguished  from  the 
second  sound.  In  advanced  cases  of  dilatation,  more  especi- 
ally dilatation  of  the  right  ventricle,  the  first  sound  is  extremely 
weak  or  almost  imperceptible,  and  is  often  replaced  by  a  sys- 
tolic murmur  due  to  mitral  or  tricuspid  regurgitation.  When 
the  dilatation  is  limited  to  the  right  ventricle,  the  sounds  of 
the  left  heart  may  be  normal,  and  vice  versa,  should  the  dila- 
tation be  limited  to  the  left  ventricle  (a  condition  which  is 
rather  of  theoretical  than  practical  importance,  for  dilatation 
of  the  left  ventricle  is  almost  always  associated  with  some 
dilatation  of  the  right),  the  first  sound  derived  from  the  right 
heart  might  be  normal. 

The  character  of  the  second  sound  varies  considerably  in 
different  cases.  In  dilatation  of  the  left  ventricle,  the  result 
of  mitral  regurgitation,  for  example,  the  aortic  second  sound 
is  weaker,  the  pulmonary  second  sound  louder  than  in  health  ; 
in  dilatation  of  the  left  ventricle,  the  result  of  aortic  regurgita- 
tion, the  aortic  second  sound  is  replaced  by  a  murmur,  the  pul- 
monary second  sound  is  either  normal  or  accentuated.  When 
the  right  ventricle  is  dilated,  the  pulmonary  second  sound  is 
generally  accentuated,  and  the  aortic  second  sound  usually 
weaker  than  normal.  (Accentuation  of  the  pulmonary  second 
sound  is  very  generally  present  in  the  earlier  stages  of  right- 
sided  dilatation  due  to  obstruction  in  front ;  in  the  final  stages, 
when  the  dilatation  is  considerable,  the  tricuspid  incompetent, 
and  the  right  ventricle  injecting  little  blood  into  the  pulmon- 
ary artery,  the  pulmonary  second  sound  is  much  less  loud 
than  in  the  earlier  stages  of  the  case.)  These  variations, 
which  depend,  of  course,  upon  the  condition  of  the  aortic 
and  pulmonary  valve  segments,  the  amount  of  blood  which  is 
being  injected  into  the  aorta  and  pulmonary  artery  respec- 
tively, and  the  resistance  in  the  arterial  and  pulmonary  circu- 
lations, will  be   readily  understood,  if  the   reader  will  again 


62  2  Diseases  of  the  Heart. 

refer  to  the  details  given  in  the  earlier  parts  of  this  work. 
(See  pages  145  and  146.) 

The  systolic  portion  of  the  cardiograph  tracing  is  unsus- 
tained,  the  summit  pointed,  and  the  up-stroke,  which  represents 
the  commencement  of  the  ventricular  systole,  followed  by  a 
rapid  fall.     (See  fig.  254.) 


Fig.  254.  —  Cardiogram  in  a  case  of  cxoplithalinic  :^oiire. — {After  Galabin.') 

'Rebecca  S.,  set.  20.  Mitral  regurgitation  combined  with  exophthalmic 
goitre.  Heart  dilated  and  hypertrophied.  Pulse  no.' — {Guy's  Hospital Kepoj-ts, 
1S75,  p.  314). 

The  radial  pulse  in  cardiac  dilatation  is,  as  a  rule,  quicker 
than  in  health,  small,  weak,  and  very  often  irregular  or  inter- 
mittent. In  extreme  conditions  of  dilatation  of  the  left  ven- 
tricle, the  frequency  of  the  pulse  is  often  less  than  the  frequency 
of  the  cardiac  contractions,  many  of  the  pulse  waves  being  too 
feeble  to  reach  the  wrist.  When  the  dilatation  is  combined 
with  much  hypertrophy,  as  it  usually  is  in  aortic  regurgitation 
for  example,  the  characters  of  the  radial  pulse  are  of  course 
quite  different. 

Diagnosis. — The  diagnosis  of  dilatation  of  the  heart  is 
more  difficult  than  the  diagnosis  of  cardiac  hypertrophy,  for 
there  are  several  conditions  which  may  simulate  an  enlarged 
and  zveak  heart — notably  effusion  into  the  sac  of  the  pericar- 
dium— but  few  which  are  likely  to  be  confounded  with  an 
enlarged  and  strojig  {i.e.  a  hypertrophied)  heart. 

Given  the  presence  of  increased  dulness  over  the  praecordial 
region,  the  steps  in  the  diagnosis  of  cardiac  hypertrophy  and 
cardiac  dilatation  are  the  same  up  to  a  certain  point : — 

Step  No.  I. — Is  the  increased  dulness  over  tJic  prcecordiuin 


Diagnosis  of  Cardiac  Dilatation.  623 

derived  from  the  heart  itself,  or  is  it  due  to  the  presence  of  some 
non-resonant  substance  in  contact  zvith  the  organ  ? 

As  a  rule  there  is  little  difficulty  in  coming  to  a  correct 
conclusion  on  this  point.  As  we  have  previously  seen,  the 
chief  pathological  conditions  which  give  rise  to  dulness  in 
the  neighbourhood  of  the  heart,  are  : — 

(a)  Consolidations  of  the  adjacent  portions  of  the  lungs 
(apoplectic,  pneumonic,  tubercular,  sarcomatous,  etc.) 

(b)  Fluid  in  the  pleural  cavity. 

(c)  Enlargement  of  the  liver. 

(d)  Tumours,  collections  of  fat,  or  inflammatory  deposits 
in  the  anterior  mediastinum. 

(e)  Aneurism  of  the  first  portion  of  the  aortic  arch. 

Now  in  most  of  these  conditions — in  the  vast  majority 
of  cases  met  with  in  practice — the  increased  dulness  is  not 
confined  to  the  limits  of  the  praecordia,  but  extends  often 
for  a  considerable  distance  into  the  surrounding  regions  of 
the  chest.^  In  many  cases  too,  it  does  not  conform  to  the 
shape  of  the  dulness  which  results  from  an  enlargement  of 
the  heart  or  pericardium.^ 

There  are,  too,  as  a  rule,  other  symptoms  and  physical 
signs  indicative  of  the  cause  of  the  dulness.  In  consolida- 
tions of  the  lung,  for  example,  cough,  expectoration,  and 
alterations  of  the  respiratory  murmur  over  the  seat  of  the 
dulness  (tubular  breathing,  rales,  etc.),  would  probably  be 
present. 

In  addition  to  those  positive  facts,  the  negative  evidence 
— that  there  are  no  signs  nor  symptoms  of  disease  of  the 
heart  or  pericardium — confirms  the  diagnosis. 

The  points,  then,  to  which  attention  should  be  directed,  in 

'  Dulness,  resulting  from  a  limited  consolidation  of  those  portions  of  the  lungs 
in  contact  with  the  heart,  might  of  course  be  limited  to  the  prcecordia.  In  such  a 
case  the  other  physical  signs  and  symptoms  (negative  and  positive)  would  be  quite 
sufficient  to  determine  the  diagnosis. 

^  It  would  be  extremely  difficult,  indeed  in  many  cases  impossible,  to  dis- 
tinguish the  dulness  due  to  a  small  tumour  or  inflammatory  accumulation  in  the 
anterior  mediastinum,  from  the  dulness  which  results  from  enlargement  of  the 
heart  or  pericardium.  Fortunately  limited  tumours  of  this  description  are  rare, 
and  the  difficulty  in  diagnosis  is  therefore  seldom  met  with  in  practice. 


624  Diseases  of  the  Heart. 

order  to  come   to  a  conclusion   as   to   the   first   step   in  the 
diagnosis,  are  : — 

1.  The  extent  and  outline  of  the  dulness. 

2.  The  presence  of  symptoms  or  physical  signs  indicative 
of  disease  of  the  adjacent  parts. 

3.  The  condition  of  the  heart  and  pericardium,  as  deter- 
mined by  other  methods  of  investigation. 

Step  No.  2. — If  the  dulness  is  directly  derived  from  the  heart 
itself  does  it  result  from  increased  exposure  {i.e.  appa^'ent 
enlargement),  or  from  actual  increase  in  the  size  of  the  organ  f 

By  far  the  most  common  cause  of  '  increased  exposure '  of 
the  heart  is  retraction  of  the  anterior  margins  of  the  lungs,  a 
condition  which  usually  results  from  pleurisy  or  cirrhosis. 

In  seeking  then  to  decide  whether  the  increased  dulness 
is  due  to  apparent  or  actual  enlargement  of  the  organ, 
attention  must  be  particularly  directed  to  the  condition  of 
the  lungs.  A  history  of  previous  pleurisy  ;  the  fact  that  the 
anterior  margins  of  the  lungs  are  fixed  by  adhesions,  and  do 
not  expand  and  cover  up  the  heart  during  inspiration — a 
point  which  can  be  determined  by  percussion  and  ausculta- 
tion, during  inspiration  and  expiration  respectively  ;  or,  the 
presence  of  symptoms  and  signs  of  cirrhosis,  phthisis,  etc., 
would  of  course  be  in  favour  of  increased  exposure  (apparent 
enlargement) — an  opinion  which  would  be  confirmed  by  the 
absence  of  symptoms  and  signs  of  pericardial  or  cardiac 
disease,  or  of  any  extra-cardiac  cause  of  enlargement  of  the 
heart,  such  as  cirrhosis  of  the  kidney  or  atheroma. 

But  while  these  are  the  points  to  which  attention  should 
be  directed,  in  order  to  make  a  diagnosis,  it  must  be  con- 
fessed that  a  positive  opinion  cannot  always  be  arrived  at ; 
and  it  is  still  more  difficult  to  exclude  any  enlargement  of 
the  heart  itself,  in  those  cases  in  which  the  increased  exposure 
is  due  to  forward  displacement  of  the  organ.  In  many  of 
these  cases  the  heart  is  actually  enlarged  as  well  as  dis- 
placed ;  and  in  those  cases  in  which  there  is  no  enlargement 
of  the  organ,  the  strong  cardiac  impulse  which  may  be  very 
noticeable,  and  the  presence  of  intra-cardiac  murmurs,  which 
may  be    produced    by  pressure    alterations    at    the   valvular 


Diagnosis  of  Cardiac  Dilatation.  625 

orifices,  may  make  it  impossible  to  exclude  all  cardiac 
hypertrophy.  In  cases  of  this  description  therefore  (which,  as 
I  have  previously  remarked,  are  extremely  rare),  a  positive 
opinion  that  the  increased  dulness  is  due  to  forward  dis- 
placement, and  not  to  enlargement  of  the  heart  itself,  could 
only  be  ventured  upon  when  : — 

(a)  There  is  distinct  evidence  of  an  aneurism  or  tumour 
behind  the  heart,  i.e.  of  the  presence  of  an  efficient  cause  of 
forward  displacement. 

(b)  There  are  no  signs  nor  symptoms  of  cardiac  disease  ; 
and  no  extra-cardiac  cause  of  enlargement,  such  as  chronic 
Bright's  disease. 

Step  No.  3. — If  the  dulness  is  due  to  an  actjial  increase  in 
the  size  of  the  organ,  does  it  result  from  fluid  in  the  sac  of  the 
pericardium,  or  from  enlargement  of  the  heart  itself? 

The  differential  diagnosis  of  pericarditis  with  effusion,  and 
of  hypertrophy  of  the  heart,  seldom  presents  any  difficulty. 
The    chief  points    of   distinction    are    given    in    Table    VII., 

P-  334- 

The  differential  diagnosis  of  dilatation  of  the  heart  and 
pericarditis  with  effusion,  is  often  most  difficult,  but  can 
usually  be  determined  by  attention  to  the  outline  of  the 
cardiac  dulness,  the  position  of  the  cardiac  impulse,  and  its 
relation  to  the  left  apex  beat,  the  presence  or  absence  of  peri- 
cardial friction,  the  presence  or  absence  of  fever,  the  history 
of  the  case,  and  the  associated  diseased  conditions.  The  points 
of  distinction  are  considered  in  detail  in  Table  VI.,  p.  333. 

Step  No.  4. — If  the  increased  dulness  is  due  to  enlargement 
of  the  heart  itself  is  the  enlaigement  general  or  partial,  and  is 
the  heart  hypertrophied  or  dilated? 

In  trying  to  determine  whether  the  enlargement  of  the 
heart  is  general  or  partial,  and  what  particular  cavity  or  cavi- 
ties are  affected,  we  observe  : — 

I.  The  cause  of  the  enlargement. — When,  for  example,  the 
cause  of  the  enlargement  is  incompetence  of  the  aortic  valves, 
we  know  that  the  left  ventricle  must  be  affected,  and  that  the 

R   R 


626  Diseases  of  tJic  Heart. 

left  auricle  and  right  side  arc,  in  many  cases,  affected  in  the 
later  stages  of  the  case.  If,  again,  chronic  bronchitis  and  em- 
physema arc  the  primary  cause  of  the  cardiac  enlargement,  the 
right  cavities  arc  first  and  most  affected,  although,  as  I  have 
previously  pointed  out,  the  left  ventricle  may  subsequently 
become  hypertrophied. 

2.  The  position  and  character  of  the  cardiac  impulse  and 
apex  beat. — When,  for  example,  the  left  ventricle  is  hypertro- 
phied, the  impulse  and  apex  beat  are  well  defined,  and  arc 
displaced  downwards  and  to  the  left.  When  the  right  ventricle 
is  affected,  the  impulse  is  carried  downwards  and  to  the  right. 
It  is,  however,  unnecessary  to  go  into  details,  since  all  of  these 
points  have  been  fully  considered  in  describing  hypertrophy 
and  dilatation  of  the  different  cardiac  cavities, 

3.  The  position  and  ont/ijie  of  the  cardiac  dulness. — This,  as 
will  at  once  be  understood  from  what  has  been  stated  in  de- 
scribing the  physical  signs  of  hypertrophy  and  dilatation,  is  an 
extremely  important  means  of  determining  the  part  of  the 
heart  which  is  enlarged. 

4.  The  character  of  the  radial  pulse. — (See  physical  signs  of 
hypertrophy  and  dilatation.) 

5.  TJie  comparative  degree  of  iutensitj'  of  the  aortic  and  pul- 
monary second  sounds. — (See  physical  signs  of  hypertrophy  and 
dilatation.) 

The  differential  diagnosis  of  JiypcrtropJiy  and  dilatation. — 
Hypertrophy  and  dilatation  are,  as  I  have  so  frequently  stated, 
very  generally  combined  ;  in  many  cases,  therefore,  the  heart 
cannot  be  said,  in  strict  language,  to  be  hypertrophied  or  dilated, 
for  it  is  both.  As  a  matter  of  practical  convenience,  however, 
we  are  in  the  habit  of  terming  an  enlarged  heart,  in  which 
hypertrophy  predominates  considerably  over  dilatation,  a 
hypertrophied  heart,  and  vice  versa  an  enlarged  heart  in 
which  dilatation  is  the  most  conspicuous  condition,  we  term  a 
dilated  heart,  even  although  it  may  at  the  same  time  be  to 
some  extent  hypertrophied.  The  reader,  who  has  attentively 
studied  the  physical  signs  detailed  under  the  head  of  hyper- 
trophy and  dilatation   respectively,  will  have  no  difficult}-  in 


Prognosis  of  Cardiac  Dilatation.  627 

distinguishing-  a  case  of  pure  hypertrophy  from  a  case  of  pure 
dilatation.  I  need  not,  therefore,  repeat  the  points  of  distinc- 
tion between  the  two  conditions.  I  must,  however,  again 
insist  upon  the  necessity  of  taking  into  account  the  condition 
of  the  lungs,  and  not  mistaking  an  enlarged  heart  which  is 
extensively  overlapped  by  an  emphysematous  lung  for  an  en- 
larged weak  {i.e.  dilated)  organ. 

Prognosis. — Speaking  generally,  it  may  be  stated  that  dila- 
tation is  an  unfavourable  condition,  and  that  the  prognosis 
of  dilatation  is  bad.  Each  case  must,  however,  be  judged  on 
its  own  merits.  The  most  important  point  in  trying  to  form 
an  opinion  as  to  the  future  progress  of  the  case,  is  to  determine 
the  exact  cause  of  the  dilatation.  If  the  cause  can  be  removed, 
the  dilatation,  in  many  cases,  disappears,  and  a  cure  is  effected. 
The  dilatation,  which  is  due  to  the  fatty  degeneration  of  chlo- 
rosis, is  almost  certainly  curable  ;  that  met  with  in  progressive 
pernicious  anaemia  can,  in  many  cases,  also  be  completely  re- 
moved by  treatment.  Dilatation  and  embarrassment  of  the 
right  heart  are  often  seen  as  temporary  results  of  bronchitis. 
It  is,  however,  unnecessary  to  quote  further  examples.  Let 
me,  however,  again  insist  upon  the  fundamental  importance  of 
trying  to  determine  the  exact  nature  of  the  cause  of  the  cardiac 
lesion,  and  the  exact  structural  condition  of  the  cardiac  muscle. 
It  is  only  after  having  satisfied  himself  on  these  points  that 
the  observer  is  in  a  position  to  give  an  intelligent  opinion  as 
to  the  future  progress  of  the  case.  The  complications  and 
associated  pathological  conditions  are,  of  course,  also  to  be 
carefully  investigated,  and  all  the  other  points  which  have 
been  detailed  in  speaking  of  the  prognosis  of  cardiac  valvular 
lesions  attended  to.  In  short,  the  physician  must  here,  as  in 
every  other  disease,  endeavour  to  take  a  broad,  comprehensive, 
and  all-round  view  of  the  case. 

Trcaiinciit. — The  treatment  of  cardiac  dilatation  is  practi- 
cally identical  with  the  treatment  of  cardiac  valvular  lesions. 
The  first  indication  is  to  endeavour  to  remove  the  cause — 
whether  it  be  some  structural  change  in  the  cardiac  muscle,  or 


628  Diseases  of  the  Heart. 

a  mechanical  cause  of  increased  intra-cardiac  tension,  or  both. 
In  the  second  place,  the  organ  must,  so  far  as  possible,  be 
placed  at  rest,  and  all  causes  of  increased  vascular  tension 
(both  in  the  systemic  and  pulmonary  circulations),  and  of 
cardiac  excitement,  carefully  avoided.  In  the  third  place, 
cardiac  tonics  and  stimulants  must  be  administered  in  accord- 
ance with  the  needs  of  each  individual  case.  In  every  case, 
the  general  health  is  to  be  maintained  in  the  highest  possible 
state  of  efficiency.  In  the  fourtJi  place,  engorgement  of  the 
venous  system,  and  all  its  secondary  results,  whether  in  the 
lungs  or  organs  behind  the  right  heart,  must  be  treated  in  the 
manner  recommended  in  speaking  of  mitral  lesions.  (The 
treatment  of  many  cases  of  dilatation  is  identical  with  the 
treatment  of  mitral  lesions.     See  page  463.) 


ATROPHY   OF   THE   HEART. 

Definition. — An  atrophied  heart  may  be  defined  as  a  heart 
which  is  decreased  in  weight  and  often  also  in  size,  in  conse- 
quence of  wasting  or  atrophy  of  its  muscular  fibres. 

This  definition  does  not  include  all  cases  in  which  the 
muscular  tissue  of  the  heart  is  wasted  ;  in  many  cases  of 
fibroid  degeneration  and  fatty  infiltration,  for  example,  the 
muscular  fibres  are  in  places  wasted,  but  the  weight  of  the 
heart  is,  as  a  rule,  fully  up  to  or  even  beyond  the  average  ;  in 
cases  of  this  description  the  atrophy  is,  as  a  rule,  local  and 
limited  in  distribution,  though  cases  of  fatty  infiltration  are 
occasionally  met  with  in  which  the  greater  part  of  the  mus- 
cular tissue  throughout  the  heart  is  atrophied  and  replaced 
by  fat. 

There  are,  in  short,  two  distinct  forms  of  cardiac  atrophy. 
In  one,  which  includes  the  cases  embraced  in  my  definition, 
the  atrophy  is  part  and  parcel  of  a  general  atrophy  ;  in  this 
form  the  whole  organ  is  affected,  though  the  wasting  may  be 
more  advanced  in  the  left  than  in  the  right  heart.  In  these 
cases  there  is  no  disease  of  the  heart  itself. 

In  the  second  form,  the  atrophy  is,  as  a  rule,  localised, 
and  is  the  direct  result  of  some  pathological  change  in  the 


Etiology  and  Pathology  of  AtropJiy  of  t lie  Heart.  629 

heart  itself,  such  as  fibroid  degeneration,  fatty  infiltration, 
fatty  degeneration,  disease  of  the  coronary  arteries.  In 
the  former  there  are,  as  we  shall  presently  see,  no  cardiac 
symptoms  ;  in  the  latter,  cardiac  symptoms  are  usually  pro- 
minent. Cases  included  in  the  latter  group  are  not  covered 
by  the  following  description,  for,  as  I  have  already  remarked, 
it  is  seldom  that  in  them  the  weight  of  the  heart  is  below 
the  average. 

Aitiology  and  Pathology. — Atrophy  of  the  heart  is  some- 
times congenital,  but  much  more  frequently  acquired. 

The  congenital  form  is  more  common  in  women  than  in 
men,  and  is  usually  associated  with  imperfect  development 
of  the  aorta  and  other  parts  of  the  vascular  apparatus  ;  the 
general  growth  of  the  system  is  usually  retarded,  and  the 
sexual  organs  often  in  a  rudimentary  condition. 

The  chief  points  which  distinguish  the  congenital  from  the 
acquired  form  of  atrophy  are  : — 

(i)  The  fact  that  the  diminished  size  of  the  heart  is  not 
necessarily  associated  with  general  emaciation. 

(2)  The  condition  of  the  pericardial  covering  and  of  the 
blood  vessels  on  the  exterior  of  the  organ.  In  the  congenital 
form  the  myocardium  fills,  as  it  were,  its  pericardial  covering, 
and  the  vessels  on  the  exterior  of  the  heart  differ  in  no 
way  from  those  of  the  normal  organ.  In  the  acquired  form, 
on  the  contrary,  the  muscular  substance  is  too  small,  so  to 
speak,  for  its  vascular  and  pericardial  coverings,  for  fibrous 
tissue  and  vessels  do  not  atrophy  to  the  same  extent  as 
muscular  tissue  ;  the  pericardial  covering,  more  especially  at 
the  apex  of  the  organ,  is  thrown  into  wrinkles  and  folds,  and 
the  vessels  on  the  surface  of  the  atrophied  organ  stand  pro- 
minently out,  and  are  much  more  tortuous  than  normal.  In 
the  congenital  form,  again,  the  usual  amount  of  sub-pericardial 
fat  is  present,  whereas  in  the  acquired  form  it  is  generally 
much  diminished,  or  has  entirely  disappeared.^ 

'  It  must,  of  course,  be  remembered  that  in  many  persons,  more  especially  in 
young  subjects,  there  is  little  or  no  fat  on  the  exterior  of  the  healthy,  normal, 
heart. 


630  Diseases  of  the  Heart. 

The  acquired  form  of  atrophy,  included  in  the  definition 
given  above  {i.e.  in  which  the  weight  of  the  heart  is  decreased), 
is  usually  the  result  of  some  general  constitutional  state  or 
local  disease  which  very  slowly  and  gradually  produces  ema- 
ciation, diminishes  the  total  amount  of  blood  in  the  body,  and 
precludes  active  bodily  exercise.  The  conditions  which,  above 
all  others,  fulfil  these  requirements,  are  stricture  of  the  oeso- 
phagus and  cancer  of  the  pylorus.  Patients  affected  with 
these  diseases  often  die  slowly  from  inanition,  after  lying  at 
rest  in  bed  for  long  periods  of  time.  Cancer  of  the  pylorus 
is,  in  fact,  as  Louis  long  ago  pointed  out,  the  disease  in  which 
the  heart  becomes  smaller  than  in  any  other  condition. 

In  many  cases  of  phthisis,  too,  the  heart  weighs  less  than 
normal,  and  is  distinctly  atrophied  ;  the  wasting  is  never,  how- 
ever, so  great  as  it  is  in  cancer  of  the  pylorus,  for  in  those 
cases  which  run  a  xcxy  chronic  course,  i.e.  cases  of  fibroid 
phthisis,  the  obstruction  to  the  passage  of  the  blood  through 
the  lungs  necessitates  over-action  on  the  part  of  the  right  ven- 
tricle, in  consequence  of  which  the  weight  of  the  heart  is  to  a 
large  extent  maintained  ;  and  in  cases  which  run  a  rapid 
course,  the  patient  docs  not  live  sufficiently  long  to  permit  of 
extreme  atrophy  taking  place  ;  the  same  cause,  too,  which 
prevents  atrophy  in  chronic  cases,  viz.,  over-action  of  the 
heart,  is  also  present  in  acute  cases,  though  in  a  less  degree. 
(In  acute  cases  there  is  not  so  much  obstruction  to  the  passage 
of  the  blood  through  the  lungs  as  in  cases  of  fibroid  phthisis, 
but  another  factor  which  necessitates  over-action  comes  into 
play,  viz.  increased  frequency  of  contraction,  and  it  is  more 
marked,  the  more  rapid  the  progress  of  the  case.) 

In  diabetes  mellitus,  in  cases  of  prolonged  suppuration,  and 
in  many  other  chronic  conditions  in  which  there  is  much  ema- 
ciation, the  heart  shares  in  the  general  wasting.  In  uncom- 
plicated cases  of  waxy  disease  of  the  kidneys,  the  heart  is 
usually  smaller  than  normal,  a  point  of  some  interest,  when 
it  is  remembered  that  in  other  varieties  of  Bright's  di.sease, 
more  especially  in  the  cirrhotic  form,  the  opposite  condition, 
viz.  hypertrophy,  occurs. 

The  essential  characteristic  of  an  atrophied  heart,  using  the 


Fig.  255. — Atrophy  of  the  heart,  seen  from  the  front.     (Exact  size.) 

The  heart  is  suspended  by  the  auricle.  The  patient,  a  woman  set.  45,  died  after 
a  very  lingering  illness  from  cancer  of  the  pylorus.  When  in  health  she  was  well 
nourished  though  never  fat ;  her  height  was  5  feet  4  inches. 

Weight  of  the  heart  =  2  oz.,  12  drs.,  11  grs.  (Av.). 

a,  points  to  the  aorta;  p,  to  the  pulmonary  artery. 


Fig.  256. — Atrophy  of  the  heart,  seen  from  behind.     (^Exact  size.) 

The  patient,  a  woman  set.  45,  died  after  a  very  lingering  illness  from  cancer  of 
the  pylorus.  When  in  health  she  was  well  nourished,  though  never  fat;  her  height 
was  5  feet  4  inches. 

Weight  of  the  heart=2  oz.,  12  drs.,  11  grs.  (Av.). 
a,  points  to  the  aorta. 


yEtiology  and  PatJiology  of  Atrophy  of  tJie  Heai't.  6 


o 


term  in  accordance  with  the  definition  given  above,  is  its  dim- 
inished weight.  Dr  Church  exhibited  before  the  Pathological 
Society  of  London  the  heart  of  an  adult,  a^t.  47  (who  died 
of  cancer  of  the  pylorus),  which  weighed  3  oz.  i  drachm. 
The  heart,  which  is  represented  in  figures  255,  256,  is  still 
smaller,  for  it  only  weighs  2  oz.  12  drs.  1 1  grs.  (avoirdupois); 
it  was  removed  from  the  body  of  a  female,  at.  45,  the  mother 
of  several  children,  who  was  under  my  care  for  many  months, 
and  who  died  from  cancer  of  the  pylorus.  When  in  health 
she  was  well  nourished,  though  never  fat ;  her  height  was 
5  ft.  4  in.  The  case  was  one  of  very  gradual  starvation  ;  I 
have  never  seen  a  more  extreme  state  of  emaciation,  every 
particle  of  fat,  and  almost  all  the  muscular  tissue  in  the  body 
having  disappeared. 

In  typical  cases  of  cardiac  atrophy  the  heart  looks  smaller 
than  natural.  This  is,  however,  by  no  means  always  the  case. 
In  some  instances,  which  have  come  under  my  own  observa- 
tion, the  heart  appeared  of  normal  size  ivJien  the  cavities  were 
relaxed  and  distended  icith  blood.  It  is,  I  think,  possible 
(though  not  in  simple  atrophy  from  disuse  and  emaciation 
such  as  I  am  now  describing)  that  an  atrophied  heart  may 
sometimes  be  larger  than  normal  in  consequence  of  dilatation 
of  its  cavities.  I  cannot  however  say  that  any  example  has 
come  under  my  own  obsen-ation.  The  general  rule  is,  I 
think,  for  the  cardiac  cavities  when  relaxed  and  distended 
with  blood  to  be  of  normal  size  or  even  less,  and  for  the 
whole  heart  when  contracted  and  empty  of  blood  to  be 
smaller  than  natural. 

On  microscopical  examination,  the  muscular  fibres  may 
present  few  alterations  from  the  normal.  In  the  extra- 
ordinary example  represented  in  figs.  255,  256,  the  individual 
fibres  are  diminished  in  size  (in  breadth) — a  change  which  has 
been  described  by  previous  writers — and  they  contain  pigment 
granules  ;  in  short,  the  microscopical  appearances  correspond 
to  the  condition  which  has  been  termed  brown  atrophy.  In 
some  cases  of  cardiac  atrophy,  more  especially  in  phthisis  and 
other  conditions  attended  with  pyrexia,  some  of  the  fibres  may 
be  fatty,  or  in  a  condition  of  cloudy  swelling. 


632  Diseases  of  the  Heart. 

Symptoms. — In  the  most  perfect  examples  of  atrophy  of 
the  heart,  such  as  occur  in  cancer  of  the  pylorus  and  phthisis, 
there  are  no  cardiac  symptoms  ;  the  heart  is  still  equal  to  the 
work  which  it  has  to  do,  and  has  simply  adapted  itself,  so  to 
speak,  to  the  nature  of  its  surroundings,  the  atrophy  is  in  fact 
one  of  disuse,  the  volume  of  blood  is  diminished,  and  the 
patient  being  precluded  from  any  active  exertion,  the  work  of 
the  cardiac  pump  is  reduced  to  a  minimum. 

Physical  signs. — In  well-marked  cases,  the  cardiac  impulse 
is  extremely  feeble  or  altogether  effaced  ;  the  precordial  dul- 
ness,  both  superficial  and  deep,  is  much  diminished,  in  extreme 
cases  it  may  be  altogether  effaced  even  during  expiration;^  the 
cardiac  sounds  are  in  some  cases  normal,  but  usually  weaker 
than  in  health.  In  cases  of  phthisis  the  pulmonary  second 
sound  is  usually  more  distinct  than  the  aortic,  it  may  be 
accentuated.  The  radial  pulse  is  small  and  weak  ;  in  phthisi- 
cal cases  its  frequency  is  increased  ;  in  those  cases  in  which 
the  atrophy  is  due  to  chronic  wasting  disease  unaccompanied 
by  fever,  it  may  be  slower  than  normal. 

Diagnosis. — The  positive  diagnosis  of  an  atrophied  heart 
is  attended  with  considerable  difficulty ;  for  a  weak  heart  which 
is  extensively  overlapped  by  lung  cannot  be  distinguished  from 
a  heart  which  is  atrophied. 

Atrophy  of  the  heart  may  be  suspected  with  considerable 
probability  when  the  patient  is  much  emaciated,  when  the 
cardiac  impulse  is  feeble  or  absent,  the  praecordial  dulness  in 
expiration  effaced,  the  heart  sounds  feeble,  and  the  pulse  small 
and  weak.  If,  in  addition,  the  obser\-er  can  satisfy  himself 
that  the  lungs  are  not  emphysematous  (a  matter,  be  it  ob- 
served, of  extreme  difficulty  in  some  cases),  a  positive  diagnosis 
of  cardiac  atrophy  could  probably  be  ventured  upon. 

'  In  many  cases  in  which  the  heart  is  atrophied  the  lungs  are  emphysematous. 
In  phthisis  the  anterior  margin  of  the  left  lung  may  of  course  be  consolidated,  and 
in  consequence  of  this  fact,  and  of  the  over-distention  of  the  right  heart  which 
is  often  present,  there  may  be  at  least  the  normal  amount  of  proecordial  dulness 
even  when  the  heart  is  somewhat  atrophied. 


Fatty  Heart.  633 

Prognosis. — The  prognosis  entirely  depends  upon  the 
nature  of  the  primary  disease  with  which  the  atrophy  is  asso- 
ciated. The  condition  of  the  heart  is  unimportant,  for  if  we 
could  cure  the  cancer  of  the  pylorus,  the  phthisis  or  other  pri- 
mary affection,  the  heart  would  readapt  itself  to  its  surround- 
ings, and  the  atrophy  would  disappear.  (This  statement  does 
not  of  course  apply  to  those  cases  in  which  the  atrophy  is 
associated  with  structural  lesions  of  the  cardiac  walls,  such  as 
fibroid  degeneration  ;  the  prognosis  of  cases  of  this  nature 
is  considered  in  other  parts  of  this  work.) 

Treatment. — Atrophy  of  the  heart  due  to  disuse,  and  asso- 
ciated with  general  emaciation,  does  not  call  for  any  special 
treatment.  Our  therapeutic  measures  must  be  entirely  directed 
to  the  primary  lesion,  and  to  improving  the  general  state  of 
nutrition. 

FATTY   HEART. 

Under  the  term  fatty  heart,  two  distinct  pathological  con- 
ditions are  included.  In  the  one — -fatty  inji/tration  or  fattj 
overgroivtJi — the  fatty  cells,  which  are  normally  present  in  the 
sub-pericardial  connective  tissue,  increase  in  numbers,  and  the 
cells  of  the  connective  tissue  of  the  myocardium  become  in- 
flated with  oil,  so  that  fatty  cells  are  found  in  the  substance  of 
the  myocardium  between  the  muscular  elements.  In  the 
other,  which  is  termed  fatty  degeneration,  oil  is  deposited 
within  the  muscular  fibres  themselves  in  the  form  of  very 
minute  (microscopical)  molecules  and  globules.  The  two 
conditions  (fatty  infiltration  and  fatty  degeneration)  are  not 
unfrequently  combined,  but  since  they  are  distinct  processes, 
and  are  often  met  with  independently,  they  must  be  con- 
sidered separately. 


FATTY   INFILTRATION   OR   FATTY   OVERGROWTH. 

Definition. — An  excessive  development  of  the  sub-peri- 
cardial fat,  with,  in  many  cases,  the  development  of  fat  cells 
between  the  muscular  fibres  of  the  myocardium. 


634  Diseases  of  the  Heart. 

yEtiology. — With  rare  exceptions  fatty  infiltration  is  part 
and  parcel  of  a  general  condition  in  which  the  fat  cells 
through  the  body  undergo  excessive  development.  All  the 
conditions,  therefore,  which  produce  general  obesity,  are 
causes  of  fatty  infiltration  of  the  heart.  In  some  persons  and 
in  some  families,  the  tendency  to  excessive  formation  of  fat 
is  hereditary;  more  frequently  the  condition  is  acquired  and  is 
due  to  rich  feeding,  especially  over-indulgence  in  fat-forming 
foods,  such  as  fatty,  saccharine,  and  starchy  articles  of  diet,  and 
in  alcoholics,  sweet  ale,  porter,  rich  sweet  wines  in  particular. 
Inactivity  and  a  sedentary  mode  of  life  are  also  important 
causes  of  the  condition.  Fatty  infiltration  of  the  heart  is  more 
common  in  men  than  in  women,  and  is  more  frequently  met 
with  in  the  upper  ranks  of  society  than  in  the  lower  classes. 

PatJioIogy  and patJiological pJiysiology.- — In  all  well  nourished 
individuals  some  fat  is  present  on  the  exterior  of  the  heart. 
Its  amount  varies  very  greatly  in  different  cases,  and  it  is  only 
when  it  becomes  distinctly  excessive  that  it  can  be  properly 
called  a  disease.  Fat  cells  are  found  in  the  sub-pericardial 
connective  tissue,  and  are  collected  more  particularly  in  the 
furrows  and  depressions  on  the  surface  of  the  heart.  Even  at 
time  of  birth,  fat  cells  are  present  in  the  auriculo-ventricular 
grooves  and  around  the  base  of  the  great  vessels  ;  they  form 
an  elastic  cushion  or  pad  which  adapts  itself  to  the  ever-vary- 
ing movements  of  the  adjacent  parts.  In  well  nourished 
adults,  and  more  particularly  in  fat  persons,  the  sub-peri- 
cardial fat  undergoes  considerable  increase,  and  deposits  of  fat 
are  seen  on  the  surface  of  the  heart,  more  especially  on  the 
anterior  surface  of  the  right  ventricle.  When  this  sub-peri- 
cardial fat  is  in  considerable  excess,  i.e.  in  cases  to  which  the 
term  fatty  overgrowth  may  be  correctly  applied,  large  masses 
of  fat  fill  the  grooves  and  furrows  and  a  thick  layer  of  fat 
covers  the  surface  of  the  organ  ;  the  anterior  surface  of  the 
right  heart  is  first  and  most  affected,  but  in  advanced  cases, 
the  whole  heart  may  be  encased  in  a  fatty  covering.  This 
appearance  is  well  seen  in  the  preparation  represented  in  fig. 
260  ;  in  it  a  layer  of  fat,  at  least  half  an  inch  thick,  is  situated 


PatJiology  of  Fatty  Injilti-ation. 


635 


on  the  exterior  of  the  right  ventricle.  When  the  cardiac  fat 
is  in  great  excess,  it  is  not  confined  to  the  surface  of  the  heart, 
but  is  found  in  the  fibrous  septa  between  the  muscular  fibres 
of  the  myocardium  (see  fig.  257)  ;  in  some  cases,  the  whole 


Fig.   257. — Fatty  infiltration  of  the  heart  from  a  section  through  the 
wall  of  the  right  auricle. 

thickness  of  the  myocardium  is  invaded,  and  it  is  said  that 
the  papillary  muscles  are  sometimes  implicated.  The  fat 
cells  encroach,  as  it  were,  upon  the  normal  territory  of  the 
myocardium,  and,  in  consequence  of  the  pressure  which  they 
exercise,  may  produce  atrophy  and  degeneration  of  the  mus- 
cular elements.  In  advanced  cases  of  fatty  infiltration,  the 
much  more  serious  condition,  fatty  degeneration,  is  generally 
present ;  in  some  cases,  more  especially  those  in  which  it  is 
limited  to  special  parts  of  the  heart,  the  fatty  degeneration  is 
due  to  imperfect  blood  supply,  the  result  of  disease  of  the 
coronary  arteries.  This  is  not  in  the  least  surprising,  when  we 
remember  how  much  more  frequently  fatty  overgrowth  is 
found  in  old  than  in  young  people  ;  the  cardiac  and  arterial 
changes  are,  in  fact,  in  many  cases,  the  common  result  of  a 
general  structural  decay. 

The  effects  of  fatty  overgrowth  vary  with  its  extent,  and 
more  especially  with  the  condition  of  the  cardiac  muscle. 


636  Diseases  of  the  Heart. 

Sytnptoms. — In  slight  degrees  of  fatty  infiltration,  there  are 
no  symptoms  nor  signs  suggestive  of  cardiac  disease.  Stout 
people,  whose  hearts  are  covered  with  an  excess  of  fat,  are  less 
capable  of  active  exertion  than  thin  people,  and  are  more  or 
less  '  short  of  wind,'  they  bear  any  excessive  strain  or  acute 
illness  badly;  but  many  stout  people  whose  hearts  are  doubt- 
less covered  with  an  excess  of  fat  enjoy  good  health  and  lead 
active  lives.  It  is  only,  however,  when  the  myocardium  is 
invaded  and  the  muscular  substance  of  the  heart  becomes 
atrophied  or  degenerated,  that  symptoms  of  defective  and 
embarrassed  circulation  arise. 

In  advanced  cases  of  fatty  infiltration,  the  symptoms  arc 
identical  with  those  of  fatty  degeneration,  which  will  be  pre- 
sently considered. 

Physical  signs. —  Slight  degrees  of  fatty  overgrowth  do  not 
produce  any  perceptible  alteration  in  the  physical  condition 
of  the  heart.  In  advanced  cases  the  cardiac  impulse  is  feeble, 
it  may  be  quite  imperceptible  when  the  patient  is  lying  on  his 
back,  but  it  can  usually  be  felt  when  he  leans  forward  or 
turns  on  to  his  left  side.  In  some  cases,  the  apex  beat  and 
cardiac  impulse,  are  entirely  absent. 

The  percussion  dulness  is,  as  a  rule,  somewhat  increased, 
but  this  point  is  often  very  difficult  to  verify  for  the  excessive 
quantity  of  fat,  both  on  the  outside  of  the  pericardial  sac,  i.e. 
in  the  anterior  mediastinum,  and  in  the  subcutaneous  tissue 
of  the  chest  wall,  makes  it  extremely  difficult  to  define  the 
exact  limits  of  the  heart.  (The  excess  of  mediastinal  and 
subcutaneous  fat  is  also  in  part  the  cause  of  the  diminished 
impulse  and  feeble  sounds.) 

The  cardiac  sounds  are  faint  and  indistinct ;  in  some  cases 
almost  imperceptible.  In  those  cases  in  which  the  fatty  over- 
growth is  associated  with  other  cardiac  lesions,  such,  for 
instance,  as  valvular  disease,  the  character  of  the  heart  sounds 
will,  of  course,  be  modified. 

In  the  slighter  degrees  of  fatty  overgrowth,  the  pulse  is  of 
good  volume  and  strength,  in  fact  quite  normal.  In  advanced 
cases,  it  is  small,  weak,  and  sometimes  irregular  ;  its  frequency 


Diagnosis  of  Fatty  Infilti'ation.  637 

varies,  in  some  cases  it  is  quicker,  in  others  decidedly  slower 
than  in  health. 


Diagnosis. — The  diagnosis  of  fatty  overgrowth  is  often 
difficult,  sometimes  impossible.  In  fat  persons  we  may,  even 
in  the  absence  of  any  symptoms  and  signs  of  cardiac  derange- 
ment, with  much  probability  suspect,  or  even  with  some  con- 
fidence predict  the  presence  of  an  increased  quantity  of  sub- 
pericardial  fat,  for  we  know  as  the  result  of  pathological 
experience  that  a  considerable  increase  of  the  subcutaneous 
fat  is  very  generally,  if  not  invariably,  attended  with  an 
increased  deposit  of  fat  on  the  exterior  of  the  heart. 

In  advanced  stages  of  fatty  infiltration,  when  the  action  of 
the  heart  is  weak,  we  may  positively  diagnose  the  condition 
when  the  patient  is  obese,  and  when  we  can  satisfy  our- 
selves that  no  other  cause  for  the  cardiac  weakness  is  present. 
In  very  fat  persons  it  is  difficult  (as  I  have  mentioned 
under  the  physical  signs)  to  ascertain  with  exactitude  the 
size  and  strength  of  the  heart  by  palpating,  percussing,  and 
auscultating  the  precordial  region.  The  condition  of  the 
radial  pulse  is,  in  such  circumstances,  the  best  guide  on  which 
we  can  rely. 

Fatty  infiltration  in  its  more  advanced  stages  cannot  be 
distinguished  from  fatty  degeneration ;  indeed,  as  I  have 
already  pointed  out,  the  two  conditions  are  usually  com- 
bined. 

Prognosis. — A  slight  excess  of  sub-pericardial  fat  is  of  no 
consequence  whatever.  A  large  excess  embarrasses  the  action 
of  the  heart,  but  provided  that  it  is  not  attended  with  symp- 
toms and  signs  of  cardiac  weakness,  i.e.  provided  that  the 
myocardium  is  not  infiltrated,  and  that  the  muscular  fibres  are 
not  degenerated,  it  is  not  necessarily  a  serious  condition.  It 
must,  however,  be  remembered  that  a  heart  which  is  loaded 
with  fat  is  heavily  handicapped  in  any  acute  illness  or  when 
any  serious  strain  is  thrown  upon  it. 

When  the  muscular  tissue  is  degenerated  (i.e.  when  symp- 
toms and  signs  of  cardiac  weakness  are  present)  the  prognosis 


638  Diseases  of  the  Heart. 

is  much  more  unfavourable,  and  is  identical  with  that  of 
fatty  degeneration.  Sudden  death  may  occur  from  syncope 
or  rupture  of  the  heart.  When  fatty  infiltration  is  associated 
with  atheroma  of  the  superficial  arteries,  and  presumably 
therefore  with  disease  of  the  coronary  arteries,  the  prognosis 
is  also  unfavourable. 

Trt'atment. — The  objects  of  treatment  are  to  limit  the 
formation  of  fat,  to  promote  the  absorption  of  the  fatty 
deposit  on  the  heart,  and  to  invigorate  the  cardiac  muscle. 
The  general  health  must  be  kept  in  the  highest  possible 
state  of  efficiency,  the  diet  strictly  regulated,  starchy  and 
fatty  foods  being  so  far  as  is  compatible  with  the  main- 
tenance of  good  health  omitted  from  the  dietary  altogether, 
sweet  ale,  porter,  and  sweet  wines  should  be  prohibited  ;  if 
any  stimulant  is  required  a  little  claret  or  whisky  and  water 
may  be  allowed.  As  much  active  outdoor  exercise,  as  is 
possible,  short  of  producing  fatigue  or  dyspnoea,  should  be 
recommended  ;  walking  exercise  in  a  dry,  moderately  cold 
and  invigorating  climate  is  best.  Hill  climbing  or  anything, 
such  as  hurrying  for  trains,  which  throws  a  sudden  strain  on 
the  heart,  is  to  be  strictly  forbidden.  The  bowels  must  be 
kept  regular,  and  straining  at  stool  avoided,  by  the  administra- 
tion of  suitable  purgatives.  Liquor  potassae  (ten  drop  doses 
three  times  a  day)  may  be  given  to  fat  persons  with  the 
object  of  reducing  the  obese  condition.  Arsenic  is  in  many 
cases  highly  beneficial.  When  symptoms  and  signs  of  cardiac 
weakness  arise,  the  case  must  be  treated  in  accordance  with 
the  rules  which  will  presently  be  laid  down  for  the  treatment 
of  fatty  degeneration. 

FATTY   DEGENERATION. 

Definition. — A  degeneration  of  the  muscular  fibres  of  the 
heart  in  which  the  albuminoid  constituents  of  the  fibre  are 
split  up  and  microscopical  particles  of  fat  are  deposited  within 
the  muscular  fibres  ;  ultimately  the  transverse  striae  disappear, 
and  the  funcdonal  activity  of  those  muscular  fibres,  which  arc 
affected,  becomes  completely  destroyed. 


^Etiology  and  Pathology  of  Fatty  Degeneration.   639 

Etiology  and  Pathology. — The  muscular  fibres  of  the  heart 
are  very  liable  to  be  attacked  by  fatty  degeneration,  and  the 
condition  is  met  with  in  a  great  variety  of  affections.  All  con- 
ditions which  interfere  with  the  supply  of  oxygen  to  the 
muscular  tissue,  and  Avhich  seriously  derange  its  nutrition, 
seem  to  produce  fatty  degeneration.  Some  of  these  condi- 
tions are  general ;  others  local.  In  chlorosis,  progressive 
pernicious  anaemia,  and,  in  fact,  in  all  conditions  of  profound 
anaemia,  fatty  degeneration  of  the  heart  is  developed.  It  is 
common  as  the  result  of  local  defects  in  the  blood  supply, 
and  is  frequently  due  to  atheroma  of  the  coronary  arteries. 
It  also  occurs  in  the  later  stages  of  those  conditions  in  which 
the  removal  of  waste  products  from  the  cardiac  walls  is  inter- 
fered with — in  the  terminal  stages  of  mitral  lesions  for 
example.  It  is  met  with  in  a  very  intense  form  in  phos- 
phorus poisoning  ;  it  results  from  poisoning  by  arsenic — a 
curious  fact  when  it  is  remembered  that  arsenic  is  the  best 
remedy  for  fatty  heart.  It  is  often  associated,  as  we  have  pre- 
viously seen,  with  fatty  infiltration.  It  is  not  uncommon  as  the 
result  of  acute  pericarditis  and  acute  myocarditis,  and  accord- 
ing to  some  authorities  it  is  also  of  frequent  occurrence  in 
fibroid  degeneration  of  the  heart.  (My  experience  is  opposed 
to  this  statement,  and  agrees  with  that  of  Dr  Charlewood 
Turner,  who  failed  to  find  fatty  degeneration  in  several  typi- 
cal cases  of  fibroid  disease.  In  the  very  chronic  forms  of 
fibroid  degeneration  the  muscular  fibres  disappear  by  a  pro- 
cess of  atrophy  rather  than  by  fatty  degeneration.  In  the 
acute  and  sub-acute  forms  of  myocarditis  fatty  degenera- 
tion is  often,  I  think,  present.)  Hypertrophied  and  dilated 
hearts  are  very  liable  to  be  affected  by  fatty  degeneration. 
The  condition  occurs  as  the  result  of  long  continued  pyrexia, 
and  is  also  met  with  in  many  chronic  cachectic  conditions, 
such  as  prolonged  suppuration,  tubercular  disease,  cancer,  etc. 
Fatty  degeneration  is  not,  however,  a  constant  condition  even 
in  severe  and  typical  cases  of  this  sort.  In  the  extraordinary 
example  of  atrophy  of  the  heart,  shown  in  figs.  255  and  256, 
there  is  no  fatty  degeneration,  so  far  as  I  have  been  able  to 
ascertain. 


640  Diseases  of  tJie  Heart. 

Fatty  degeneration  of  the  heart  may  occur  at  any  age  and 
in  either  sex.  The  anaemic  form  is  more  common  in  women 
than  in  men,  and  in  young  than  in  old  people.  (Chlorosis, 
which  is  the  most  common  cause  of  this  form  of  fatty  de- 
generation, is  of  course  a  disease  of  the  female  sex  and  of 
young  women.  Progressive  pernicious  anaemia  is  also  a 
disease  of  early  and  middle  adult  life,  and  is,  according  to 
some  observers,  somewhat  more  common  in  women  than  in 
men.) 

The  idiopathic  form  of  fatty  degeneration,  as  it  is  some- 
times called  {i.e.  that  form  which  is  so  frequently  associated 
with  disease  of  the  coronary  arteries),  is  more  common  in 
males  than  in  females,  and  is  essentially  a  disease  of  later 
life.  It  has  sometimes  been  called  the  senile  form  of  fatty 
degeneration.  The  form  of  fatty  degeneration  which  is  com- 
bined with  fatty  infiltration  is  sometimes  also  called  idio- 
pathic. 

A  heart  w^hich  is  affected  with  fatty  degeneration  is,  as  a 
rule,  somewhat  larger  than  normal.  In  those  cases  in  which 
the  fatty  change  attacks  a  heart  which  was  previously  hyper- 
trophied  and  dilated,  the  increase  in  size  may  of  course  be 
great ;  when  the  fatty  degeneration  is  the  sole  cardiac  lesion 
the  increase  is  seldom  considerable,  and  is,  for  the  most  part, 
only  apparent,  i.e.  due  to  the  flabby  and  relaxed  condition  in 
which  the  organ  is  found  after  death.  In  cases  of  this  de- 
scription the  heart  is,  as  a  rule,  somewhat  dilated  ;  in  some 
cases,  as  in  chlorosis  and  progressive  pernicious  anaemia  for 
example,  some  hypertropy  is  also  present ;  should  the  fatty 
degeneration  follow  upon  long  continued  suppuration,  tuber- 
cular disease,  etc.,  the  organ  may  be  somewhat  atrophied. 

Its  colo2ir  is  paler  than  normal,  usually  of  a  fawn  yellow 
or  pale  buff;  in  some  cases,  notably  in  pernicious  anaemia, 
the  fatty  change  is  irregularly  distributed  amongst  the 
muscular  fibres  ;  the  interior  of  the  heart  appears  to  be  dotted 
over  or  speckled  with  little  yellow  points,  which  give  it  a 
mottled  appearance,  not  unlike  the  breast  of  a  thrush,  to 
which  it  has  been  compared. 

The  consistency  is  softer  than   normal,  and   in   advanced 


Pathology  of  Fatty  Degeneration.  641 

cases  the  wall  of  the  heart  can  be  readily  broken  down  by 
the  finger.  The  left  ventricle  is  the  part  of  the  heart  which 
is  most  liable  to  be  attacked,  the  papillary  muscles  being  in 
many  cases  profoundly  affected  ;  the  right  ventricle  is  the 
next  part  to  suffer,  then  the  left  auricle,  and  last  of  all  the 
right  auricle. 

When  the  lesion  is  due  to  disease  of  the  coronary  artery, 
the  fatty  change  is  usually  more  localised,  and  may  be  limited 
to  small  portions  of  the  organ,  the  exact  position  depends  of 
course  upon  the  distribution  of  the  branch  of  the  artery  which 
happens  to  be  affected. 

On  microscopical  examination,  the  affected  muscular  fibres 
are  seen  to  contain  little  molecules  of  oil  wdiich  stain  black 
with  perosmic  acid  ;  these  molecules  are  very  minute,  and 
are,  for  the  most  part,  singularly  uniform  in  size  ;  in  some 
cases  they  coalesce  and  form  minute  globules  which  seldom, 
however,  exceed  the  size  of  half  a  red  blood  corpuscle.  The 
fatty  molecules  are  sometimes  arranged  in  rows,  but  are 
usually  distributed  in  an  irregular  manner  throughout  the 
whole  thickness  of  the  fibre  ;  as  the  change  progresses,  the 
transverse  striae  become  indistinct  and  finally  disappear,  the 
whole  fibre  ultimately  becoming  filled  with  little  oily  par- 
ticles.    (See  fig.  258.) 


Fig.  258. — Muscular  fibres  cf  the  heart  in  a  case  of  fatty  degeneration. 
rt,  a,  a,  fibres  in  which  the  fatty  change  is  just  commencing ;  b,  b,  fibres  in  which 


it  is  far  advanced. 
S    S 


642  Diseases  of  the  Heart. 

Muscular  fibres  aflfected  with  fatty  degeneration  arc  much 
more  brittle  than  healthy  ones,  and  readily  break  up  trans- 
versely into  short  fragments. 

In  fatty  hearts  it  is  not  at  all  uncommon  to  find  the 
condition  which  has  been  termed  brown  atrophy,  in  which 
pigment  particles  arc  deposited  around,  more  particularly 
at  the  ends  or  poles  of  the  muscle  nuclei.  The  connective 
tissue  nuclei,  and  the  fibrous  septa  between  the  fibres  are 
sometimes  also  increased  ;  this  change  is  chiefly,  I  think, 
observed  in  hj'pertrophicd  hearts,  more  especially  in  those 
conditions,  such  as  mitral  regurgitation,  in  which  the  venous 
return  from  the  cardiac  walls  is  interfered  with.  Fat  cells 
are,  of  course,  seen  between  the  muscular  fibres,  in  those 
cases  in  which  fatty  degeneration  is  combined  with  fatty 
infiltration. 

The  functional  activity  of  a  muscular  fibre,  which  is 
affected  with  even  a  moderate  degree  of  fatty  degeneration, 
is  seriously  interfered  with  ;  in  the  final  stages  of  the  process 
the  fibre  loses  its  contractility  altogether.  In  those  cases, 
therefore,  in  which  a  large  number  of  the  muscular  fibres  arc 
affected,  and  in  which  the  change  is  widely  distributed 
throughout  the  heart,  the  cardiac  pump  is  of  necessity 
greatly  weakened.  Under  such  circumstances  we  should  of 
course  expect  the  systemic  arterial  system  to  be  under  dis- 
tended and  the  systemic  venous  system  to  be  over  distended 
with  blood  ;  and  in  chlorosis  and  progressive  pernicious 
anaemia,  in  which  affections  the  fatty  change  reaches  a  high 
degree  of  intensity  and  is  widely  distributed  throughout  the 
heart,  these  results  do  actually  occur.  In  these  affections, 
too,  the  heart  becomes  both  dilated  and  hypertrophied,  and 
relative  and  muscular  incompetence  at  the  mitral  and  tricuspid 
orifices  are  not  unfrequcntly  established. 

When  the  fatty  degeneration  is  combined  with  fatty  over- 
growth independently  of  the  anaemic  condition,  the  same 
sequence  of  events  is  often  observed. 

In  some  cases  of  fatty  degeneration,  arterial  anaemia  is  the 
only  result ;  and  dilatation  of  the  ventricles,  regurgitation  at 
the   mitral   and   tricuspid   orifices,   and    engorgement   of  the 


Pathology  of  Fatty  Degeneration.  643 

systemic  veins,  arc  not  observed.  These  dififerences  arc 
sometimes  very  difficult  to  explain.  In  some  cases  the  absence 
of  cardiac  dilatation  and  venous  engorgement  is  probably 
due  to  the  fact  that  the  fatty  change,  although  reaching  a 
high  degree  of  intensity  in  certain  fibres,  is  limited  in  dis- 
tribution, and  the  healthy  fibres,  which  remain,  are  able  to 
carry  on  the  work  of  the  circulation  provided  that  the  organ 
is  not  called  upon  to  make  any  sudden  effort.  In  others,  the 
explanation  is  probably  to  be  found  in  the  fact  that  the 
patients  are  old  people  in  .whom  the  tissue  changes  are  at 
a  minimum,  and  who  lead  tranquil,  placid  lives.  Such 
patients  suffer  little  so  long  as  they  keep  quiet,  the  slightest 
extra  exertion,  however,  brings  a  shortness  of  breath  ;  if 
they  continue  to  exert  themselves,  or,  if  in  consequence  of 
deranged  cardiac  and  vaso-motor  innervation,  or  any  other 
cause  independently  of  muscular  exertion,  the  heart  has 
continuously  to  exceed  the  quiet  minimum  of  work,  so  to 
speak,  of  which  it  is  capable,  the  other  secondary  conse- 
quences (dilatation,  venous  engorgement,  auriculo-vcntricular 
regurgitation)  would  doubtless  follow.  In  others  again,  the 
absence  of  symptoms  and  signs  of  venous  engorgement  is 
probably  due  to  the  fact  that  the  mitral  orifice  is  unyielding- 
owing  to  senile  (atheromatous)  changes  in  the  mitral  ring,  in 
consequence  of  which  relative  incompetence  of  the  mitral 
orifice  does  not  occur. 

The  extent,  and  more  particularly  the  distribution,  of  the 
fatty  change,  the  amount  of  work  which  the  heart  is  called 
upon  to  do,  the  state  of  the  mitral  ring,  and  the  condition  of 
the  cardiac  and  vaso-motor  nerve  mechanisms  seem  to  me  to 
be  the  chief  factors  to  which  we  must  look  in  order  to  explain 
the  different  results  which  are  met  with  in  these  two  classes 
of  cases.  That  the  condition  of  the  central  nervous  system 
exerts  a  most  important  influence  upon  the  secondary  results 
of  cardiac  disease  is,  I  think,  perfectly  clear.  I  have  seen,  for 
example,  a  case  in  which  the  arterial  tension  was  high,  the 
left  ventricle  hypertrophied  and  dilated,  the  mitral  valve  in- 
competent and  somewhat  contracted  the  result  of  old  rheu- 
matic disease,  the  lungs  in  a  condition  of  brown  atrophy,  the 


644  Diseases  of  tJic  Heart. 

right  ventricle  hypertrophicd  and  considerably  dilated,  and  in 
which  a  very  considerable  amount  of  fatty  degeneration  of  the 
hypertrophicd  right  and  left  ventricles  was  also  present,  in  which 
there  was  extreme  shortness  of  breath  on  exertion,  and  yet 
in  which  there  was  never  any  subcutaneous  dropsy.  Such  a 
result  can  only,  I  think,  be  explained  by  supposing  that  the 
condition  of  the  blood  and  of  the  peripheral  vessels,  probably 
in  consequence  of  some  peculiarity  in  the  nerve  or  nervo- 
muscular  tone,  prevented  the  occurrence  of  subcutaneous 
effusion. 

Symptoms  ami  physical  signs. — After  \\hat  I  have  just 
stated,  it  will  be  at  once  understood  that  there  are  several 
types  of  fatty  heart,  and  that  the  symptoms  and  physical  signs 
differ  very  materially  in  different  cases. 

The  symptoms  and  physical  signs  of  the  fatty  degeneration 
of  the  heart,  which  is  due  to  general  anaem.ia,  and  which  is 
met  with  in  its  most  typical  form  in  chlorosis  and  progressive 
pernicious  anaemia,  have  been  previously  described  in  treating 
of  mitral  regurgitation.     (See  page  441.) 

When  the  fatty  degeneration  is  combined  with  fatty  infiltra- 
tion, the  subcutaneous  fat  is  almost  invariably  well  developed, 
all  degrees  of  obesity  being  met  with  ;  the  Colour  of  the  skin 
is  usually  pale,  but  should  mitral  or  tricuspid  incompetence 
be  at  the  same  time  present,  blueness  of  the  lips  and  the 
other  external  manifestations  of  pei'ipheral  venous  engorge- 
ment may  of  course  be  present.  In  cases  of  combined  fatty 
degeneration  and  fatty  infiltration,  the  skin  often  has  a  greasy, 
unctuous  feel,  and  this  is  more  especially  the  case  when  the 
patient  is  intemperate. 

In  other  cases,  more  especially,  I  think,  in  those  in  which 
the  fatty  degeneration  depends  upon  disease  of  the  coronary 
arteries,  the  patient  is  rather  the  reverse  of  fat ;  the  peripheral 
arteries  stand  out  prominently,  and  the  arcus  senilis  is  often 
present.  The  abdomen  is  not  unfrequently  covered  with  a 
considerable  layer  of  fat,  and  the  big,  pendulous  belly  con- 
trasts forcibly  with  the  flabby  and,  comparatively  speaking, 
attenuated   extremities,     (General   atheroma,   disease  of  the 


Symptoms  of  Fatty  Degeneration.  645 

coronary  arteries,  and  the  arcus  senilis,  are  of  course  frequently 
observed  in /at  people  whose  hearts  are  fatty.) 

The  subjects  of  fatty  degeneration  of  the  heart  are,  as  a 
rule,  incapable  of  concentrated  mental  effort  and  of  any  active 
bodily  exertion  ;  this  is  more  particularly  the  ease  when  the 
fatty  change  is  widely  distributed  throughout  the  heart. 
Cases  are,  however,  not  uncommon,  in  which  persons  who 
have  been  leading  active  and  useful  lives  suddenly  die  from 
fatty  heart.  In  these  cases  the  fatty  change  is  usually  limited 
in  distribution.  I  have  known  three  instances  in  which  pro- 
fessional men  —  two  physicians  and  one  clergyman  —  have 
suddenly  died  from  rupture  of  the  heart,  all  of  them  having 
been  actively  engaged  until  within  a  day  or  two  of  death  in 
professional  work.  In  all  of  these  cases  the  coronary  arteries 
were  atheromatous,  and  the  fatal  rupture  was  apparently  due 
to  arrested  blood  supply  and  acute  localised  softening. 

A  'sinking'  sensation  is  sometimes  complained  of  in  the 
pit  of  the  epigastrium  ;  in  some  cases  there  is  actual  pain  in 
the  region  of  the  heart  ;  occasionally  true  attacks  of  angina 
pectoris  occur. 

Shortness  of  breath  on  exertion  is  usually  a  prominent 
symptom,  and  exertion  often  causes  a  dry,  irritable,  cough. 
In  advanced  cases,  the  dyspnoea  may  become  constant. 
'  Cheyne-Stokes '  respiration  sometimes  precedes  the  fatal 
issue. 

Some  of  the  more  prominent  symptoms  are  due  to  anaemia 
of  the  brain.  The  memory  is,  in  many  cases,  impaired  ;  the 
patient  loses  his  former  decision  of  character  and  '  nerve,'  and 
may  become  wayward  and  irritable.  Vertigo  is  a  common 
symptom  ;  and  in  advanced  cases,  fainting  is  not  unfrequently 
observed,  getting  up  from  the  recumbent  to  the  sitting  or 
standing  position,  or  raising  the  head  suddenly,  may  bring  on  an 
attack  of  syncope.  Pseudo-apoplectic  attacks,  in  which  the 
patient  remains  unconscious  for  some  time,  are  met  with  in 
some  cases.  When  fatty  degeneration  is  combined  with  other 
cardiac  lesions,  such,  for  example,  as  mitral  regurgitation, 
other  symptoms,  which  I  need  not  here  detail,  are  of  course 
present. 


646  Diseases  of  tJie  Heart. 

heart.  The  cardiac  impulse  is  feeble,  and  in  some  cases,  more 
especially  in  those  in  which  the  chest  wall  is  covered  by  a  thick- 
layer  of  fat,  altogether  effaced.  The  impulse,  when  perceptible, 
is  more  diffused  than  in  health.  The  praecordial  dulness  may 
be  quite  normal  or  slightly  increased  ;  in  those  cases  in  which 
the  heart  is  dilated  or  hypertrophied  from  associated  disease 
the  increase  may,  of  course,  be  considerable.  In  typical  cases, 
and  more  especially  when  the  heart  is  acting  quietly,  the  first 
sound  is  feeble,  muffled,  and  distant  ;  its  duration  is  consider- 
ably shorter  than  in  health.  These  characters  are  not,  how- 
ever, observed  in  all  cases.  In  chlorosis,  for  example,  the 
heart  is  very  irritable  and  easily  excited,  and  the  first  sound, 
although  shorter  than  in  health,  is  usually  quite  distinct,  its 
tone  is  raised,  in  fact  it  may  present  all  the  characters  which 
have  been  described  under  the  head  of  cardiac  dilatation. 
The  same  character  of  the  first  sound  may  be  present  in  other 
forms  of  fatty  degeneration  when  combined  with  dilatation. 
Mitral  and  tricuspid  systolic  murmurs  are  of  frequent  occur- 
rence, more  especially  in  anaemic  cases. 

The  characters  of  the  pulse  differ  very  considerably  in 
different  cases,  and  depend  upon  the  irritability  of  the  cardiac 
muscle,  the  presence  or  absence  of  dilatation,  and  the  condi- 
tion of  the  valvular  apparatus. 

In  some  cases  (more  especially  in  anaemic  cases  and  in 
those  in  which  the  fatty  degeneration  is  combined  with 
dilatation)  the  pulse  is  quicker  than  normal  ;  in  others  (more 
particularly,  I  think,  when  the  fatty  degeneration  is  associated 
with  general  atheroma  and  disease  of  the  coronary  arteries) 
the  pulse  frequency  is  diminished. 

In  advanced  cases  the  rhythm  is  often  irregular,  though 
exceptions  to  this  general  statement  frequently  occur.  When 
the  fatty  degeneration  is  combined  with  dilatation  and  mitral 
disease,  the  pulse  may  be  extremely  irregular,  and  some  of  the 
pulse  waves  may  fail  to  reach  the  wrist.  In  typical  cases  of 
fatty  degeneration,  the  pulse  is  small  and  extremely  weak — 
an  exception  occurs  in  chlorotic  cases,  in  the  earlier  stages  of 
which  the  arterial  tension  is  increased 

Physical  signs. — The  physical  signs  are  those  of  a  weak 


Diagnosis  of  Fatty  Degeneration,  647 

Diagnosis. — The  diagnosis  of  fatty  degeneration  of  the 
heart  is,  in  some  cases,  attended  with  great  difficulties.  In 
order  to  come  to  a  positive  conchision  we  must,  in  the  first 
place,  satisfy  ourselves  that  the  action  of  the  heart  is  perma- 
nently weak  ;  and,  in  the  second  place,  that  there  is  no  other 
cause  for  the  cardiac  weakness  (such  as  fibroid  degeneration, 
mitral  disease,  etc.). 

Too  much  importance  should  not  be  attached  to  the 
results  of  the  physical  examination  ;  for,  on  the  one  hand,  it 
is  extremely  difficult  to  determine  the  exact  physical  condi- 
tion of  the  organ  in  those  cases  in  which  the  chest  wall  is 
thickly  covered  by  subcutaneous  fat,  or  in  which  the  heart  is 
overlapped  by  emphysematous  lungs;  and,  on  the  other,  the 
agitation,  which  many  patients  experience  when  they  come 
to  consult  a  physician,  induces  overaction  of  the  heart,  in- 
creases the  intensity  of  the  cardiac  sounds  and  the  frequency 
of  the  pulse,  and  often  leads  to  the  belief  that  the  organ  is 
stronger  that  it  actually  is.  It  is  very  essential,  therefore,  in 
all  cases,  in  which  the  symptoms  are  suggestive  of  fatty  heart, 
and  particularly  in  those  cases  in  which  there  is  reason  to 
suppose  that  the  action  of  the  organ  is  modified  by  nervous 
causes,  to  examine  the  patient  more  than  onCe,  and,  as 
Professor  Gairdner  has  forcibly  pointed  out,^  under  various 
conditions  of  cardiac  action,  before  committing  ourselves  to  a 
positive  opinion.  Feeble  cardiac  impulse,  a  short  and  muffled 
first  sound,  a  weak  pulse,  and  symptoms  of  cerebral  anaemia, 
are  the  positive  facts  which  are  of  most  importance,  and  which 
enable  us  to  make  the  first  step  in  the  diagnosis,  viz.,  that  the 
heart  is  weak. 

The  second  step,  viz.,  that  the  weakness  is  due  to  fatty 
degeneration  of  the  heart,  is  chiefly  attained  by  the  method 
of  exclusion.  We  can  only  give  a  positive  diagnosis  of  fatty 
heart  when  we  are  satisfied  that  the  cardiac  weakness  is 
not  a  mere  temporary  condition,  and  when  we  have  excluded 
valvular  lesions  (more  particularly  mitral  valve  lesions),  cardiac 
dilatation,    myocarditis,   fibroid    degeneration,    and    adherent 

'   Russell  Reynolds'  System  of  Medkitie,  vol  iv.  jx  546. 


648  Diseases  of  the  Heart. 

pericardium,  in  all  of  which  conditions  the  same  indications  of 
cardiac  weakness  may  be  present. 

Fatty  degeneration  may  of  course  be  combined  with  any 
of  these  lesions,  and  in  many  cases  in  which  these  conditions 
(mitral  lesions,  cardiac  dilatation,  etc.)  are  present,  we  may, 
from  the  progress  of  the  case  and  from  the  nature  of  the 
symptoms  and  physical  signs,  have  good  reason  to  suspect  that 
the  cardiac  muscle  is  fatty.  Mere  suspicion  or  probabilit\- 
does  not,  however,  justify  a  positive  diagnosis. 

The  absence  of  any  marked  symptoms  and  signs  of 
pulmonary  and  systemic  venous  engorgement,  the  absence  of 
endocardial  murmurs,  the  fact  that  the  cardiac  muscle  does 
not  respond  well  to  cardiac  tonics  {i.e.  to  digitalis),  the  general 
condition  of  the  patient  (corpulence,  an  atheromatous  condi- 
tion of  the  superficial  arteries,  the  presence  of  an  arcus  senilis, 
a  history  of  intemperance)  are  all  strongly  in  favour  of  fatt}' 
heart,  and  enable  us  to  exclude  most  of  the  other  causes  of 
cardiac  weakness  and  defective  circulation  which  I  have  just 
mentioned. 

Mitral  lesions  sufficiently  severe  to  produce  the  symptoms 
which  are  present  in  typical  cases  of  fatty  degeneration,  such 
as  we  are  now  considering,  would  in  all  probability  be  at- 
tended with  dropsy  and  other  symptoms  and  signs  of  venous 
engorgement — mitral  murmurs  would  probably  be  present, 
and  there  would  be  distinct  evidence  of  enlargement  of  the 
right  heart.  In  advanced  stages  of  mitral  regurgitation  the 
systolic  apex  murmur  sometimes  vanishes,  but  can  almost 
invariably  be  re-established  by  the  administration  of  digitalis  ; 
in  advanced  cases  of  mitral  constriction  the  murmur  is  ver}' 
often,  usually  indeed,  absent.  Now,  in  pure  cases  of  fatty 
degeneration  (?>.  cases  uncombined  with  any  considerable 
amount  of  dilatation  or  with  mitral  or  tricuspid  regurgita- 
tion) there  are  no  symptoms  of  venous  engorgement,  or,  at 
all  events,  such  symptoms  are  slight.  There  is  little  diffi- 
culty, therefore,  in  making  a  distinction  between  pure  cases  of 
fatty  heart  and  cases  of  mitral  regurgitation. 

It  is,  in  most  cases,  impossible  to  distinguish  fatty  de- 
generation   of   the    heart    and    chronic    myocarditis ;    fibroid 


Prognosis    of  Fatiy  Degeneratioji.  649 

degeneration  sufficiently  severe  to  cause  the  symptoms  and 
physical  signs  which  characterise  advanced  cases  of  fatty 
degeneration,  would  be  more  likely  to  be  attended  with 
considerable  dilatation,  and  Avith  symptoms  and  signs  of 
venous  engorgement. 

In  women  at  the  meno-pause,  attacks  of  syncope  and 
other  indications  of  defective  circulation  are  not  uncommon. 
Should  the  patient  be  stout,  it  may  be  impossible  to  exclude 
fatty  heart.  The  diagnosis  can  only  be  made  by  watching 
the  future  progress  of  the  case. 

In  chlorosis  and  other  conditions  of  advanced  anaemia  the 
diagnosis  of  fatty  heart  can  be  positively  made,  for  we  know 
as  the  result  of  pathological  experience,  that  the  cardiac 
muscle  is  in  a  condition  of  fatty  degeneration  in  these  cases. 

Prognosis. — The  prognosis  of  fatty  degeneration  of  the 
heart  depends  upon  the  cause.  In  chlorotic  cases  the  patient 
will  almost  certainly  get  well ;  in  progressive  pernicious 
anaemia  the  prognosis  is  very  hopeful  if  arsenic  be  systemati- 
cally administered  in  the  manner  which  I  have  previously 
described.  The  fatty  degeneration  which  attends  long  con- 
tinued pyrexia  is  generally  recovered  from.  The  fatty 
degeneration  of  old  age  ;  that  which  results  from  disease  of 
the  coronary  arteries  ;  and  that  which  attacks  hearts  affected 
with  chronic  valvular  disease  or  other  permanent  structural 
lesion  (such  as  the  hypertrophy  of  chronic  Bright's  disease, 
the  hypertrophy  which  attends  emphysema,  etc.),  is  seldom, 
if  ever,  recovered  from. 

In  trying  to  form  a  forecast  of  the  probable  course  of  the 
case,  it  is  important  to  remember  that  fatty  degeneration  is  a 
frequent  cause  of  sudden  death  ;  the  fatal  result  may  be  due 
to  syncope,  rupture  of  the  heart,  or  angina  pectoris. 

Fatty  degeneration,  however  slight,  adds  very  seriously  to 
the  dangers  of  an  acute  illness.  Persons  whose  hearts  are 
fatty  bear  pain  badly,  and  are  unfavourable  subjects  for 
severe  operations.  Should  they  require  an  anaesthetic,  ether, 
or  a  mixture  of  ether  and  chloroform,  should  be  administered 
to  them.     (But  they  are  not,  in  my  opinion,  exceptional  in  this 


650  Diseases  of  tJie  Heart. 

respect,  for,  so  far  as  I  can  weigh  the  experimental  and  other 
evidence,  ether  is  a  much  safer  anaesthetic  than  chloroform  ; 
the  practical  advantages  which  attend  the  administration  of 
chloroform  do  not,  so  far  as  I  can  judge,  at  all  counterbalance 
the  greater  risks  to  which  it  subjects  the  patient.) 

Treatment. — The  treatment  of  fatty  degeneration  of  the 
heart  varies  somewhat  in  accordance  with  the  cause.  Our 
main  object  is,  of  course,  to  remove  the  condition. 

In  anaemic  cases,  iron,  arsenic,  or  a  combination  of  these 
drugs,  must  be  given,  and  the  general  treatment,  which  has 
been  previously  described  in  treating  of  mitral  regurgitation 
(see  p.  463),  carried  out.  Great  care  must  be  taken  in  these, 
and  indeed  in  all  cases  of  fatty  or  weak  heart,  to  avoid  throw- 
ing any  sudden  strain  upon  the  damaged  organ,  but  this  point 
will  be  again  referred  to  presently. 

In  the  fatty  degeneration  which  follows  a  severe  attack  of 
typhus  or  other  continued  fever,  the  treatment  must  be 
essentiall}'  tonic  ;  quinine,  iron,  and  strychnine  are  useful 
drugs.  When  the  cardiac  weakness  is  extreme  the  patient 
must  be  cautioned  against  making  any  sudden  effort  or  doing 
anything  which  is  likely  to  induce  cardiac  syncope.  The 
dietetic  and  other  measures  suitable  for  a  convalescent — and 
which  it  is  unnecessary  to  mention  here — must  of  course  be 
prescribed.  Cardiac  tonics  and  stimulants  (digitalis,  brandy, 
ammonia,  etc.),  are  required  when  the  cardiac  weakness  is 
very  great ;  and  since  the  fatty  change  may  be  established 
before  the  period  of  convalescence  is  reached,  the  remedies  may 
of  course  be  required  during  the  febrile  stage  of  the  disease. 

The  treatment  of  the  fatty  degeneration  which  is  so  often 
established  in  the  terminal  stages  of  cardiac  valvular  lesions, 
hypertrophy  of  the  heart,  etc.,  has  already  been  considered 
under  the  different  valvular  lesions. 

In  treating  the  senile  form  of  fatty  degeneration,  we  can 
seldom,  if  ever,  expect  to  remove  the  cause,  and  our  treatment 
must  therefore  be  for  the  most  part  palliative.  All  sources 
of  cardiac  strain,  or  anything  likely  to  induce  cardiac  syncope, 
must  be  carefully  guarded  against.     All  sudden  efforts  must 


I 


Treatment  of  Fatty  Degenei-ation.  651 

be  forbidden  ;  all  sources  of  mental  worry,  anxiety,  or  excite- 
ment avoided  ;  in  fact,  the  patient  must,  so  far  as  is  possible, 
considering  his  mental  disposition  and  surroundings,  be  made 
to  lead  a  quiet  and  regular  life.  The  patient  should  be 
cautioned  against  suddenly  rising  from  the  recumbent  posi- 
tion ;  warm  baths  and  powerful  purgatives  are  not  permis- 
sible in  those  cases  in  which  there  is  a  tendency  to  syncope, 
and  in  which  symptoms  of  cerebral  ansemia  are  prominent. 
The  general  health  must  be  maintained  in  the  best  possible 
state  of  efficiency.  The  diet  must  be  digestible,  but  at  the 
same  time  nutritious,  and  the  quantity  of  food  taken  at  each 
meal  should  be  strictly  moderate.  Flatulent  distention  of 
the  stomach  should,  if  possible,  be  prevented,  for  a  distended 
stomach  pushes  up  the  diaphragm  and  seriously  impedes  the 
action  of  the  heart.  A  heavy  meal  should  on  no  account  be 
taken  just  before  going  to  bed,  or  the  patient  will  be  likely  to 
wake  up  with  troublesome  dyspnoea,  or  perhaps  alarming 
symptoms  of  cardiac  failure.  I  have  known  more  than  one 
case  in  which  a  patient  who  had  taken  a  hearty  supper  awoke 
during  the  night  and  suddenly  expired,  and  in  which  the 
exciting  cause  of  the  attack  seemed  to  be  overloading  of  the 
stomach.  The  bowels  must  be  kept  regular,  and  the  con- 
dition of  the  skin  carefully  attended  to. 

Plenty  of  fresh  air  is  eminently  desirable ;  the  proper 
ventilation  of  the  rooms  in  which  the  patient  lives  during  the 
day  and  sleeps  during  the  night,  is  a  very  important  point. 
As  much  outdoor  exercise  as  is  possible,  short  of  producing 
fatigue  or  dyspnoea,  is  desirable.  Unfortunately  in  advanced 
cases,  even  gentle  Exercise  cannot  be  indulged  in.  Should 
symptoms  of  sudden  cardiac  failure  arise,  brandy,  ammonia, 
ether,  or  other  stimulant  remedies,  should  be  promptly 
administered.  Attacks  of  dyspnoea,  cardiac  pain,  angina 
pectoris,  etc.,  must  of  course  be  met  as  they  arise,  by  appro- 
priate remedies.  Arsenic,  iron,  and  strychnine  are  the  most 
useful  drugs.  In  some  cases,  more  especially  where  there  is 
associated  mitral  valvular  disease  or  cardiac  dilatation,  digi- 
talis is  of  the  greatest  service  ;  but  in  others  it  seems  useless 
or  even  prejudicial,  it  increases  the  arterial   tension,  and  so 


652  Diseases  of  the  Heart. 

throws  an  increased  strain  upon  the  heart,  witliout  (in  some 
cases)  appearing  to  produce  any  beneftcial  influence  upon 
the  damaged  cardiac  wall. 

SPONTANEOUS  RUPTURE  OF  THE  HEART. 

Etiology  and  Pathology. — Spontaneous  rupture  of  the 
heart  probably  never  occurs  Avhcn  the  organ  is  perfectly 
healthy,  but  is  always  the  result  of  disease.  It  is  occasionally, 
though  rarely,  due  to  acute  softening  of  the  cardiac  wall,  the 
result  of  acute  local  myocarditis  or  thrombosis  of  the  coronary 
artery  ;  in  most  cases  it  is  due  to  chronic  softening,  the  result 
of  fatty  changes,  both  fatty  infiltration  and  fatty  degeneration, 
but  especially  the  latter.  The  bursting  of  an  aneurism  of  the 
cardiac  wall  is  another,  but  a  very  rare,  cause  of  the  condition. 

In  the  majority  of  cases  it  is  the  wall  of  the  left  ventricle 
which  gives  way,  doubtless  in  consequence  of  the  facts  that 
the  degenerative  changes,  which  are  the  causes  of  the  rupture, 
more  frequently  involve  the  left  ventricle  than  the  other  parts 
of  the  heart,  and  that  the  blood  pressure  within  the  cavity  of 
the  left  ventricle  during  its  systole  is  much  greater  than  in  the 
other  cavities  of  the  organ.  The  rupture  is  usually  situated 
in  the  anterior  wall  of  the  ventricle  in  the  neighbourhood 
of  the  septum  ;  in  some  cases  it  is  placed  in  the  posterior 
wall ;  exceptionally  it  is  the  wall  of  the  right  ventricle  which 
gives  way.  The  burst  sometimes  occurs  when  the  patient  is 
making  a  sudden  effort,  such  as  hurrying  for  a  train,  or  strain 
at  stool ;  in  other  cases,  it  takes  place  while  he  is  at  perfect 
rest. 

The  size  of  the  rupture  varies  from  a  mere  slit  to  an  ex- 
tensive lacerated  opening;  in  some  cases,  the  external  open- 
ing {i.e.  the  opening  into  the  pericardium)  is  smaller  than  the 
internal. 

The  effect  of  the  rupture  is,  of  course,  to  allow  the  escape 
of  blood  from  the  cavity  of  the  heart  into  the  sac  of  the 
pericardium.  When  the  laceration  is  extensive  and  a  large 
quantity  of  blood  escapes,  death  may  be  instantaneous  ;  in 
other  cases,  more  especially  when  the  rupture  is  a  small  one, 
and   the    direction   of  the   rupture  oblique,  the  patient  may 


Fig.  259.    Rupture  of  the  Left  Veiitricle  seen  from  the  outside.    (^Natural  size.) 

The  heart  is  covered  by  a  thick  layer  of  fat,  which  at  the  point  a  is  five-eighths  of  an  inch 
in  thickness;  b,  muscular  substance  btmeath  the  external  layer  of  fat.  A  piece  of  whalebone  has 
been  placed  in  the  external  orifice  of  the  rupture. 


Fig.  260.    Rupture  of  the  Left  Ventrick.    (^Natural  size.) 

The  heart  has  been  bo  cut  open  that  the  septum  ventriculorum  and  the  interior  of  both 
Tentricles  are  seen.     A  piece  of  whalebone  is  inserted  into  the  rupture. 

a,  interior  of  the  aorta ;  b,  pulmonary  artery  transversely  divided ;  c,  interior  of  right 
auricle ;  d,  septum  ventriculorum ;  e,  interior  of  right  ventricle ;  f,  piece  of  whalebone  placed  in 
rupture ;  g,  layer  of  fat  ou  the  exterior  of  the  heart. 


SpontaneoiLS  Rupture  of  the  Heart.  653 

live    for   several    hours,    or    even    for    some    days,    after   the 
occurrence  of  the  accident. 


Synptojus  a}id  physical  signs. — The  occurrence  of  rupture 
of  the  heart  is  attended  with  sudden  and  severe  pain  in  the 
heart ;  if  the  patient  is  standing  or  walking  when  the  accident 
occurs,  he  will  probably  fall  to  the  ground.  In  those  cases  in 
which  death  does  not  immediately  occur,  there  are  all  the 
appearances  of  collapse,  and  in  addition  to  the  pericardial 
pain  and  oppression,  the  patient  complains  of  great  difficulty 
in  breathing.  When  the  patient  survives  sufficiently  long  to 
be  seen  by  a  physician,  the  pain,  dyspnoea,  and  collapse,  are 
usually  so  great  as  to  prohibit  a  minute  examination  of  the 
chest.  The  specimen  represented  in  figures  2^9  and  260  is 
typical,  both  as  to  its  pathological  characters  and  the  clinical 
symptoms  which  were  present  during  life.  The  history  of  the 
case  is  as  follows  : — 

A.  B.,  a  parish  patient,  set.  67,  a  big,  stout  woman  who  had  previously 
enjoyed  fair  health,  was  suddenly  seized  one  morning  on  getting  out  of 
bed  to  get  a  drink,  with  a  severe  pain  in  the  region  of  the  heart.  Her 
neighbours,  who  lived  in  the  room  beneath,  heard  her  fall  heavily  on  the 
floor,  and  on  proceeding  to  her  assistance  they  found  her  in  a  semi- 
conscious condition.  On  my  arrival  shortly  afterwards,  I  found  her 
conscious,  but  in  a  condition  of  profound  collapse  ;  skin  covered  with  a 
cold  clammy  sweat,  pupils  dilated,  voice  husky,  pulse  hardly  perceptible. 
There  was  great  difficulty  in  breathing  ;  she  had  vomited  ;  she  com- 
plained of  intense  pain  and  oppression  in  the  region  of  the  heart  ;  the 
precordial  region  was  exquisitely  tender  to  the  touch,  and  I  was  con- 
sequently unable  to  ascertain  the  extent  of  the  percussion  dulness  ;  the 
heart  sounds  were  not  heard.  Morphia  and  brandy  were  administered, 
and  a  soap  and  opium  liniment  was  applied  over  the  region  of  the  heart. 
The  patient  died  eight  hours  afterwards.  On  making  a  posi-mortc7ii 
examination  I  found  the  pericardial  sac  distended  with  black  clotted 
blood.  The  rupture  shown  in  the  drawing  was  situated  in  the  anterior 
wall  of  the  left  ventricle  close  to  the  septum.  The  internal  aperture 
was  ragged,  and  considerably  larger  than  the  external.  The  heart  was 
in  an  advanced  condition  of  fatty  infiltration,  a  layer  of  fat,  fully  half  an 
inch  thick,  being  situated  on  the  exterior  of  the  right  ventricle  At  the 
seat  of  the  rupture  the  muscular  fibres  were  in  an  advanced  condition  of 
fatty  degeneration  ;  the  coronary  arteries  were  atheromatous,  and  the 
branch  supplying  the  ruptured  part  of  the  heart  was  obstructed. 


654  Diseases  of  the  Heart. 

Diagnosis. — The  sudden  occurrence  of  severe  pain  in  the 
region  of  the  heart,  followed  by  collapse  and  difficulty  of 
breathing,  is  suggestive  of  rupture  of  the  heart.  Should  the 
patient  survive  a  sufficient  length  of  time,  it  may  be  possible 
to  detect  the  enlargement  of  the  pericardial  sac  by  means 
of  percussion. 

Prognosis. — The  prognosis  in  cases  of  spontaneous  rup- 
ture is  hopeless.  In  no  case,  so  far  as  I  know,  has  recovery 
taken  place. 

Treatment. —  Little  can  be  done  in  the  way  of  treatment. 
Morphia  should  be  given  to  allay  the  pain,  and  a  cold  anodyne 
liniment  applied  to  the  prascordial  region.  The  profound 
collapse  which,  in  many  cases,  threatens  to  prove  immediately 
fatal,  and  which  indeed  in  some  cases  does  prove  fatal,  sug- 
gests the  administration  of  stimulants  ;  but  it  is  important  to 
remember  that  remedies  which  give  increased  strength  to  the 
heart  are  injurious,  in  so  far  as  they  favour  an  increased 
quantity  of  blood  being  expelled  from  the  cardiac  cavity  into 
the  sac  of  the  pericardium.  Stimulants  should  only,  therefore, 
be  administered  in  those  cases  in  which  the  collapse  threatens 
to  prove  fatal. 

WAXY  DEGENERATION  OF  THE  HEART. 

Waxy  degeneration  of  the  heart,  which  is  not  very  un- 
common in  cases  in  which  the  lardaceous  change  is  widely 
distributed  throughout  the  body,  has  recently  been  described 
by  Professor  D.  J.  Hamilton  ;  but  since  it  is  not  characterised 
by  any  distinctive  cardiac  symptoms  or  signs,  and  is  of  patho- 
logical rather  than  of  clinical  importance,  it  is  unnecessary  to 
refer  to  it  in  detail  here.^ 

NEW  GROWTHS  IN  THE  HEART. 

^Etiology  and  Pathology.  —  The  heart  is  occasionally 
the  seat  of  new  growths  ;  primary  tumours  are  extremely 
rare,    secondary    deposits    (more    especially    cancerous    and 

^  Journal  of  .-inatoiny  and  Physiology,  Oct.  1SS3,  p.  54. 


Fio.  261.     Ttmumr  on  the  exterior  of  the  Heart.     (Natural  size.) 

The  patient  died  suddenly  a  few  days  after  delivery ;  she  had  never  complained  of  cardiac 
sympcoms. 


M'LuulCuxm.eLmolEoi 


Fie.  262.    Sarcomatous  tumours  in  the  heart.    (NatuTol  size.) 

The  walls  of  the  right  ventricle,  which  have  been  cut  open,  are  kept  apart  by  a  piece  of 
stick  (a). 

6,  tumour  on  the  exterior,  and  c,  tumour  on  the  interior  of  the  right  ventricle;  the  internal 
tumour  is  situated  immediately  below  the  tricuspid  orifice 

Copied  by  Professor  Turner's  permission  from  a  specimen  in  the  Anatomical  Museum  of  the 
Edinburgh  University. 


Nri«,.«lCu»«i»Gljii.c?Eoi» 


New  Gj^owths  in  the  Heart.  655 

sarcomatous  tumours  and  hydatid  cysts)  are  more  common. 
The  more  important  of  the  new  growths  which  have  been 
met  with  in  the  heart  are: — 

1.  Cancer. — Very  few  instances  of  primary  cancer  of  the 
heart  are  on  record ;  secondary  deposits  of  scirrhous  and  en- 
cephaloid  are  occasionally  met  with,  and  are  said  to  occur 
more  frequently  on  the  right  than  on  the  left  side  of  the  organ. 
The  cancerous  nodules  are  usually  situated  on  the  surface  of 
the  organ,  and  are  then  sub-pericardial ;  in  some  cases  they 
are  sub-endocardial;  occasionally,  though  rarely,  they  are 
embedded  in  the  myocardium.  Pericarditis  occurs  in  some 
cases  in  which  the  cancerous  nodules  are  situated  beneath  the 
visceral  pericardium,  and  is  still  more  common  when  a  cancer 
of  the  lung  or  mediastinal  tissues  makes  its  way  through  the 
parietal  layer  of  the  sac. 

2.  Sarcomata. — Various  forms  of  sarcoma  (lympho-sar- 
coma,  melanotic  sarcoma,  etc.)  have  been  met  with  in  the 
heart,  and  are  probably  more  common  than  cancer.  They 
are  usually  secondary.  The  individual  tumours  may  attain 
to  considerable  size,  as  in  the  specimen  represented  in  fig.  261. 
The  sarcomatous  nodules  may  be  situated  on  the  surface  of 
the  organ,  beneath  the  endocardium,  or  in  the  substance  of 
the  myocardium.  In  rare  cases,  a  remarkable  example  of 
which  has  just  come  under  my  notice  in  the  post-mortem 
theatre,  a  malignant  tumour  of  the  mediastinum  may  make 
its  way  through  the  wall  of  the  heart  or  down  the  superior 
vena  cava,  and  form  a  tumour  in  the  interior  of  the  heart. 
In  the  case  to  which  I  refer  the  cavity  of  the  right  auricle 
was  almost  entirely  filled  by  a  large  mass  of  new  growth. 
The  sub-pericardial  and  sub-endocardial  forms  of  cardiac 
sarcoma  are  well  seen  in  fig.  262.  Sarcomatous  tumours  on 
the  surface  of  the  heart  have  not  the  same  tendency  to  pro- 
duce pericarditis  as  cancers. 

3.  Tubercle. — Miliary  tubercles  are  occasionally,  though 
more  rarely  than  might  be  expected,  met  with  in  the  tissues 
of  the  pericardium,  and  are  always  associated  with  tubercular 
nodules  in  other  organs  ;  they  are  much  more  common  in 
children  than  in  adults  ;  some  pericarditis  is  usually  present. 


656  Diseases  of  tJic   Heart. 

Large  caseous   nodules — descried    as   tubercular — have   also 
occasionally  been  met  with. 

4.  Syphilitic  guutuiata. — Though  extremely  rare,  these  are 
probably  more  common  in  the  heart  than  is  usually  supposed  ; 
they  are  seldom  seen  in  the  gumma  stage  ;  limited  fibroid 
patches  in  the  cardiac  walls  are,  in  many  cases,  syphilitic,  and 
are  sometimes,  I  believe,  the  scars  of  former  gummata  ;  in 
other  cases,  the  gumma  becomes  caseous  (some  of  the  caseous 
masses  formerly  described  as  tubercular  wei'e  probably  gum- 
mata) ;  in  others,  again,  the  gumma  becomes  calcified.  In 
the  heart  represented  in  fig.  196  (see  p.  479),  there  were 
several  large  calcareous  masses  in  the  substance  of  the  left 
ventricle  ;  the  patient,  who  had  suffered  from  .'^philis,  died 
from  the  rupture  of  the  aneurism  represented  in  figures  268 
and  269  ;  the  stone-like  nodules  in  the  heart  probably,  I  think, 
represent  gummata,  which  had  healed  and  undergone  cal- 
careous degeneration. 

5.  Hydatid  cysts. — -These  have  been  frequently  found  in  the 
heart  ;  no  case  has,  however,  come  under  my  own  observation. 
Of  700  cases  of  hydatid  disease  collected  by  Davaine  and 
Cobbold,^  the  hydatid  was  situated  in  the  heart  and  pul- 
monary vessels  in  25  cases.  The  cyst  may  be  placed  beneath 
the  pericardium,  in  the  substance  of  the  myocardium,  under 
the  endocardium  ;  in  some  cases  the  sac,  attached  by  a  narrow 
pedicle  to  the  endocardium,  swings  freely,  as  it  were,  in  the 
interior  of  the  organ  (usually  in  the  right  auricle  or  right 
ventricle).  The  sac  may  be  sufficiently  large  to  obstruct  the 
orifices  ;  in  some  cases  it  ruptures,  and  the  contents  are 
carried  as  emboli  to  the  lungs  (when  the  hydatid  is  situated 
in  the  right  cavities)  or  to  the  peripheral  organs  when  the 
cyst  ruptures  into  the  left  heart. 

6.  Simple  cysts. — Some  writers  mention  these  as  occur- 
ring in  the  heart.  They  are,  however,  extremely  rare,  and 
their  exact  pathological  significance  has  still  to  be  worked  out. 
Ur  Ogle  met  with  a  blood  cyst  in  the  pericardium  which  he 
thinks  was  due  to  the  rupture  of  one  of  the  branches  of  the 

'  Parasites. — A  Treatise  on  the  Entozoa  of  Man  and  Animals,  by  Dr  Spencer 
Cobbold,  p.  122. 


y'j^S'  -'^ 


I 


Fig.  263. — Cys<  iw  <Ae  anterior  wall  of  the  left  auricle.     (^Natural  size.') 
The  specimen  is  referred  to  in  the  text.     (See  page  656.) 


WUcnJCu-m.-gLiimcUoi 


JVciu  GrowtJis  ill  tJie  Heart.  657 

coronary  artery.^  In  the  specimen  represented  in  fig.  263, 
which  I  met  with  in  \.\\q  post-mortem  theatre  of  the  Edinburgh 
Royal  Infirmary  during  the  past  session  (the  specimen  oc- 
curred in  a  case  of  Dr  Wylhe's,  with  whose  permission  it  is 
represented  here)  a  cyst  the  size  of  a  small  orange,  con- 
taining partly  fluid  and  partly  clotted  blood,  is  situated  in 
the  anterior  wall  of  the  left  auricle,  i.e.  between  the  auricle 
and  the  posterior  surface  of  the  base  of  the  aorta.  The  aortic 
orifice  was  extremely  stenosed,  the  two  cusps  (there  were  only 
two  cusps)  being  converted  into  thick,  dense,  calcareous 
masses;  there  had  apparently  been  old  ulceration  at  the  base 
of  the  cusps,  and  between  them  a  depression,  which  passed 
backwards  in  the  direction  of  the  cyst,  existed,  and  seemed  to 
represent  an  old  ulcer.  The  coronary  arteries  which  passed 
round  the  wall  of  the  cyst  were  pervious.  The  cyst  was 
probably  I  think,  an  aneurism  which  had  originally  communi- 
cated with  the  left  ventricle  at  the  point  of  depression,  situated 
between  and  just  below  the  two  segments  of  the  aortic  valve  ; 
the  orifice  had  become  obliterated,  and  the  sac  partly  filled 
up  by  deposits  of  laminated  fibrine. 

7.  Fibroid  tiunoiirs. — Vegetations  which  look  like  fibroid 
growths  are  occasionally  met  with  ;  they  usually  spring  from 
the  mitral  valve-ring,  and  grow  upwards  into  the  cavity  of 
the  left  auricle.  A  very  beautiful  specimen,  which  seemed 
to  be  of  this  description,  came  under  my  observation  in  the 
post-mortem  theatre  of  the  Edinburgh  Royal  Infirmary  a  few 
months  ago. 

Symptoms  and  physical  signs. — In  many  cases  the  presence 
of  the  new  growth  is  not  manifested  either  by  symptoms  or 
physical  signs  ;  in  fact,  in  most  cases  tumours  of  the  heart 
are  of  pathological  rather  than  of  clinical  interest. 

In  some  cases  (more  especially  in  the  cancerous  and 
tubercular  forms),  pericarditis  is  established.  In  others  (more 
especially  in  the  case  of  hydatid  tumours  projecting  into  the 
cardiac  cavities,  sub-endocardial  sarcomata,  syphilitic  gum- 
mata  in  the  ventricular  walls  near  the  insertion  of  the  valves, 

'  Transactions  of  the  Pathological  Society  of  Londo!:,  vol.  ix.  p.  165. 
T   T 


658  Diseases  of  the  Heart. 

and  the  rare  fibroid  growth  which  springs  from  the  mitral 
ring)  the  tumour  is  so  situated  as  to  produce  obstruction  or 
to  interfere  with  the  perfect  closure  of  one  or  other  of  the 
valvular  orifices.  In  such  cases  the  usual  symptoms  and 
signs  of  valvular  disease  may  be  present. 

Diagnosis.- — Primary  tumours  in  the  heart  cannot  be 
diagnosed  during  life.  Secondary  deposits  may  be  suspected 
when  the  symptoms  or  physical  signs  of  pericarditis  or 
valvular  disease  arise  in  the  course  of  a  case  in  which  there 
are  (or  have  been)  new  growths  of  a  malignant  or  hydatid 
character  in  other  parts  of  the  body. 

Prognosis.- — It  is  unnecessary  to  dwell  on  the  prognosis, 
since  it  is  in  most  cases  impossible  to  recognise  the  presence 
of  the  new  growth  during  life. 

Treatment. — In  those  cases  in  which  pericarditis  or  valvular 
disease  is  present,  the  treatment  which  has  been  previously 
recommended  for  those  conditions  must  be  practised.  When 
there  is  reason  to  suspect  that  the  cardiac  derangement 
depends  on  tubercle  or  syphilis,  the  remedies  which  arc 
appropriate  for  those  affections  must  be  administered.  W^hen 
there  is  reason  to  suppose  that  the  heart  is  affected  witli 
cancerous  or  sarcomatous  growths,  the  systematic  adminis- 
tration of  arsenic  should  be  tried. 


The  Cardiac  Neuroses.  659 


CHAPTER     VII. 

THE   CARDIAC    NEUROSES.     PALPITATION.     INTERMITTENT   ACTION. 
ANGINA  PECTORIS. 

Cardiac  Neuroses. 

Under  the  head  of  cardiac  neuroses  are  included  a  variety 
of  conditions,  the  most  prominent  feature  of  which  is  derange- 
ment of  the  nervous  mechanism  of  the  heart.  In  some  cases, 
the  motor  and  co-ordinating  part  of  the  mechanism  is  affected  ; 
in  others,  the  sensory  part  is  implicated  ;  while  in  others  both 
the  motor  and  sensory  functions  are  involved. 

In  many  cases,  the  heart  itself  is  perfectly  healthy  ;  the 
cardiac  affection  is  then  purely  functional.  In  other  cases,  the 
neurotic  derangement  is  either  caused  by,  or  is  associated 
with,  structural  lesions  in  the  heart,  aorta,  or  pericardium. 

Palpitation,  irregular  and  intermittent  action,  and  cardiac 
pain,  are  the  most  important  external  manifestations  of  these 
neurotic  disturbances. 

PALPITATION    OF   THE   HEART. 

Definition. —  Palpitation  of  the  heart  is  a  symptom  not  a 
disease.  It  consists  of  excessive  action  of  the  organ.  The 
frequency  of  the  heart's  contractions  is  usually,  but  not  always, 
increased  ;  the  cardiac  action,  which  is  in  some  cases  irregular 
or  intermittent,  is  vividly,  and  sometimes  painfully,  perceptible 
to  the  patient.     The  condition  is  essentially  paroxysmal. 

Etiology  and  Pathology. — There  are  two  great  forms  of 
palpitation,  viz.,  organic  and  neurotic  or  functional. 


66o  Diseases  of  the  Heart. 

1.  Organic  palpitation. — In  this  form  the  heart  is  diseased, 
and  the  palpitation  is  usually  an  indication  of  cardiac  weak- 
ness. Whenever,  in  fact,  the  heart  (whether  healthy  or 
diseased)  is  called  upon  to  make  a  greater  effort  than  its 
reserve  force  is  equal  to,  palpitation  is  apt  to  be  experienced. 
Palpitation  is  consequently  a  common  symptom  in  cardiac 
dilatation,  and  in  cases  of  failing  hypertrophy.  The  exciting 
cause  of  the  palpitation  is  very  commonly  a  sudden  increase 
of  the  peripheral  resistance,  the  result  of  muscular  effort,  vaso- 
motor constriction,  etc.  In  other  cases,  organic  palpitation 
is  the  result  of  excessive  irritability  of  the  cardiac  muscle. 
This  is  notably  the  case  in  the  fatty  degeneration  of  ansemia, 
in  which  condition  attacks  of  palpitation  are  extremely  com- 
mon and  are  at  once  produced  by  any  exertion. 

2.  Neurotic  palpitation. — In  typical  cases  of  neurotic  pal- 
pitation there  is  no  organic  cardiac  lesion,  but  the  deranged 
action  is  due  to  disturbance,  either  direct  or  reflex,  of  the 
motor  and  co-ordinating  mechanism  of  the  heart. 

3.  In  a  third  group  of  cases  the  organic  and  neurotic  forms 
of  palpitation  are  combined.  In  anaemia,  for  example,  the 
cardiac  nerves  as  well  as  the  cardiac  muscle  are  unduly 
irritable,  and  palpitation  is  very  readily  produced  by  mental 
and  emotional  causes  i^i.e.  causes  acting  through  the  nervous 
system)  as  well  as  by  muscular  effort  and  other  conditions 
which  throw  an  increased  strain  upon  the  irritable  and 
weakened  heart. 

The  following  description  will  be  limited  more  especially 
to  the  neurotic  form  of  palpitation,  though  I  shall  incidentally 
refer  to  the  organic  variety. 

Neurotic  Palpitation. 

^-Etiology  and  Pathology. — Neurotic  palpitation  is  a  very 
common  condition,  and  is  of  considerable  practical  importance, 
for  it  not  only  causes  discomfort  and  anxiety  at  the  time  of 
the  attack,  but  persons  who  are  affected  by  it  are  very  apt  to 
suppose  that  the  heart  is  organically  diseased,  and  to  labour 
under  the  fear  of  sudden  death.  Neurotic  palpitation  is 
frequently  observed   in   healthy  persons,   more   especially   in 


Pathology  of  Neurotic  Palpitation.  66 1 

emotional  and  excitable  individuals.  Persons  of  a  phleg- 
matic disposition,  and  those  who  have  strong  control  over 
themselves,  i.e.  '  cool  people,'  are  not  often  affected  by  it 
when  in  health. 

Pathologically  we  find  that  anything  which  lowers  the 
nerve  tone  and  power  of  self-control  predisposes  to  this  form 
of  palpitation.  It  is  apt  to  occur  during  convalesence  from 
severe  disease  ;  it  is  met  with  in  all  forms  of  ansemia  ;  seden- 
tary occupations,  unhealthy  surroundings,  insufficient  food, 
bad  ventilation,  want  of  sun-light,  are  therefore  powerful  pre- 
disposing causes ;  it  is  particularly  apt  to  arise  in  conse- 
quence of  sexual  excesses,  mental  worry  and  anxiety,  over 
work  and  loss  of  sleep.  Prolonged  muscular  effort,  more 
especially  when  combined  with  great  mental  excitement  and 
insufficient  food,  sometimes  gives  rise  to  it — witness  the  fre- 
quency of'  irritable  heart'  and  palpitation  in  the  soldiers  who 
took  part  in  the  great  American  War.  Palpitation  is  very 
common  in  hysteria  ;  is  frequently  caused  by  over  indulgence 
in  tea  and  tobacco  ;  is  frequently  seen  in  connection  with 
dyspepsia  and  gout ;  is  a  very  prominent  symptom  in  ex- 
ophthalmic goitre  (Grave's  disease)  ;  and  is  sometimes  pro- 
duced reflexly  by  uterine  and  ovarian  derangements,  worms 
in  the  intestine,  etc. ;  it  is  too  of  common  occurrence  in  the 
early  stage  of  pulmonary  phthisis. 

Neurotic  palpitation  is  much  more  common  in  early  adult 
life  than  at  any  other  period ;  and  is  more  common  in  women 
than  in  men,  though  very  severe  palpitation  is  frequently  met 
with  in  young  males,  usually,  I  believe,  as  a  result  of  sexual 
excesses  and  over  indulgence  in  tobacco.  The  exact  manner 
in  which  the  nervous  mechanism  is  deranged  cannot  alwa}'s 
be  ascertained.  Theoretically  we  may  suppose  that  palpita- 
tion may  be  due  to  the  following  conditions  : — 

1.  Excessive  stimulation  or  over  irritability  of  the  ganglia 
and  nerves  in  the  heart  itself  This  is  probably,  in  part  at 
least,  the  cause  of  the  palpitation  of  anaemia,  and  of  that  due 
to  tea  and  tobacco. 

2.  Excessive  action  of  the  sympathetic — the  cardiac  ac- 
celerator. 


662  Diseases  of  the  Heart. 

3.  Defective  action  of  the  vagus — the  inhibitory  nerve  of 
the  heart. 

In  exophthalmic  goitre  there  is  probably  an  organic  lesion 
of  the  cervical  sympathetic  ;  in  other  cases,  as  for  example, 
in  locomotor  ataxia,  in  which  attacks  of  palpitation  analogous 
to  the  so  called  gastric  crises  are  sometimes  observed,  the 
lesion  (which  produces  the  palpitation)  is  probably  situated 
in  the  cervical  portion  of  the  spinal  cord,  or  in  the  medulla 
oblongata.  In  other  cases,  as  for  example  in  hysteria,  the 
higher  (cerebral)  centres  are  at  fault  ;  while  in  others,  the 
derangement  is  reflex  and  due  to  peripheral  irritation. 

The  exciting  cause  of  neurotic  palpitation  is  very  generally 
a  sudden  start  or  other  form  of  emotional  disturbance.  The 
palpitation  is  usually  aggravated,  and  is  sometimes  produced 
when  the  patient's  attention  is  directed  to  the  heart.  Neurotic 
palpitation  is  rarely  followed  by  any  permanent  cardiac 
lesion.  In  one  case,  which  has  come  under  my  observation, 
in  which  a  young  man  was  suddenly  attacked  during  the 
night  with  most  violent  palpitation,  slight  aortic  regurgita- 
tion subsequently  developed.  I  have  always  suspected  that 
in  that  case  one  of  the  aortic  segments  sustained  some  injury, 
possibly  a  slight  rupture,  during  the  attack. 

Dilatation  and  hypertrophy  may,  I  am  convinced,  result 
from  long  continued  palpitation.  I  have  in  several  instances 
satisfied  myself  of  the  occurrence  of  temporary  hypertrophy 
in  the  neurotic  heart  of  young  males  ;  and  dilatation  and  some 
hypertrophy  are  of  frequent  occurrence  in  the  later  stages  of 
exophthalmic  goitre.^ 

Syinptovis  and  pliysical  signs. — The  onset  of  neurotic 
palpitation  is  usually  abrupt.  In  some  cases,  the  exciting 
cause  is  something  external  to  the  organism  (a  loud  noise, 
some  cause  of  mental  or  emotional  disturbance,  etc.),  which 
produces  sudden  stimulation  of  the  sensory  cerebral  centres  ; 
in  others  the  exciting  cause  is  some  internal  irritation,  such  as 

'  In  exophthalmic  goitre  the  dilatation  is  probably  due  to  other  causes,  such,  for 
example,  as  degeneration  of  the  muscular  fibre,  and  not  altogether  to  the  excessive 
action  of  the  organ. 


Symptoms  and  Signs  of  Neurotic  Palpitation.     663 

dyspepsia  or  other  visceral  derangement.  The  attack  may 
occur  at  any  time.  Some  of  the  most  severe  cases  which  have 
come  under  my  observation  occurred  during  the  night,  the 
patient  being  awakened  by  the  violent  beating  of  the  heart. 

The  most  prominent  symptom  is  the  exaggerated  pulsation 
of  the  heart  ;  the  organ  may  be  felt  thumping  or  knocking 
against  the  chest  wall ;  in  some  cases  the  patient  hears  the 
beating  as  well  as  feels  it.  In  severe  cases,  a  feeling  of  intense 
anxiety  or  dread  is  at  the  same  time  experienced.  Some  prae- 
cordial  distress  is  often  present,  and  in  exceptional  cases,  there 
is  actual  pain  in  the  region  of  the  heart.  Violent  throbbing 
pulsation  in  the  peripheral  vessels,  noises  in  the  ears,  a  feeling 
of  tension  and  fulness  in  the  head  are  common.  The  face  is  in 
some  cases  flushed  ;  in  others  pale,  expressive  of  anxiety,  and 
perhaps  bedewed  with  clammy  sweat.  A  choking  sensation 
in  the  throat  (globus)  or  a  feeling  of  syncope  may  be  ex- 
perienced ;  difficulty  of  breathing  is  sometimes  present,  but 
true  dyspnoea  is  not  usually  observed.  (In  organic  palpita- 
tion dyspnoea  and  other  indications  of  embarrassed  venous 
circulation  are  usually  prominent  symptoms.)  When  the 
cardiac  action  is  at  the  same  time  intermittent  or  irregular; 
the  patient  is  very  sensible  of  the  altered  rhythm  of  the  heart. 
The  duration  of  the  paroxsysm  is  usually  brief,  but  repeated; 
attacks  are  apt  to  follow  one  another  at  short  intervals.  In 
some  cases,  the  attack  terminates  as  suddenly  as  it  corn- 
menced.  In  a  case,  for  instance,  which  I  have  recorded  else- 
where the  pulse  suddenly  dropped  from  1 50  to  60,  and  the 
attack  instantaneously  disappeared.  The  termination  may  be 
attended  with  a  copious  discharge  of  pale,  limpid  (hysterical) 
urine.  After  severe  attacks  the  patient  is  sometimes  much 
exhausted  ;  exceptionally  fainting  is  observed. 

During  the  paroxysm,  the  frequency  of  the  cardiac  con- 
tractions is,  as  a  rule,  much  increased,  the  pulse  may  number 
200  or  even  250  in  the  minute  ;  in  some  cases  of  organic 
palpitation  the  frequency  of  the  heart's  action  is  little  if  at  all 
increased.  On  inspection,  the  area  of  cardiac  impulse  is  seen 
to  be  increased  ;  and  violent  beating  is  felt  when  the  hand  is 
placed  over  the  praecordia.     In  exceptional  cases,  a  thrill  or 


664  Diseases  of  the  Heart. 

tremor  can  be  perceived.  The  area  of  cardiac  dulness  is 
seldom  altered  to  any  appreciable  extent.  (This  statement 
does  not  of  course  refer  to  organic  palpitation  in  which  the 
heart  is  so  frequently  dilated  or  hypertrophied).  On  ausculta- 
tion, the  first  sound  is  unusually  loud,  ringing  and  metallic  ; 
the  second  sound  is  in  some  cases  accentuated ;  but  where  the 
heart  is  acting  very  quickly  it  is  usually  less  loud  than  in 
health  or  altogether  effaced.  Basic  murmurs  are  sometimes 
observed  ;  but  occasionally  a  basic  murmur,  which  was  present 
when  the  heart  was  beating  quietly,  becomes  effaced.  (Sec 
the  case  reported  by  me  in  the  Lancet,  November  27,  1875, 
p.  764.)  The  heart's  action  and  the  pulse  are,  in  most  cases 
of  neurotic  palpitation,  regular  ;  but  irregularities  and  inter- 
mission are  not  at  all  uncommon.  In  some  cases,  the  pulse 
is  full  and  bounding  ;  in  others,  small  and  feeble.  Fulness  in 
the  veins  of  the  neck  may  be  present.^ 

Diagnosis. — In  every  case  of  palpitation  the  physician  has 
to  determine  : — 

1.  Is  the  palpitation  associated  with  organic  cardiac  disease, 
or  is  it  neurotic  in  character  1 

2.  If  organic,  what  is  the  exact  nature  of  the  cardiac  lesion  ? 

3.  If  neurotic,  what  is  the  cause  of  the  attack  "i 

Step  No.  I. — Is  the  palpitation  associated  zvit/i  organic 
cardiac  disease,  or  is  it  neurotic  ? 

In  order  to  determine  this  important  point,  attention  must 
be  directed  to  : — 

1.  The  physical  condition  of  the  heart. — The  size  of  the 
heart,  the  condition  of  the  valvular  apparatus,  and  the  state 
of  the  cardiac  muscle  (as  evidenced  by  the  physical  examina- 
tion) must  be  carefully  ascertained.  The  difficulties  which 
attend  the  recognition  of  fatty  degeneration  and  other  struc- 
tural lesions  of  the  cardiac  walls,  when  unattended  with 
valvular  disease  or  with  enlargement,  must  be  remembered. 
In  most  cases,  even  when  the  results  of  physical  examination 

'  These  statements  have  special  reference  to  neurotic  (functional)  palpitation. 
In  organic  cases  the  character  of  the  peripheral  arterial  and  venous  circulations 
depends  of  course  upon  the  nature  of  the  structural  lesion. 


Diagnosis  of  Neurotic  Palpitation.  665 

are  inconclusive,  the  other  circumstances  which  I  am  about 
to  mention  usually  enable  us  to  come  to  a  correct  conclusion. 
Repeated  careful  examinations  in  different  states  of  cardiac 
action  are,  however,  in  many  cases  necessary  before  a  positive 
opinion  can  be  formed.  In  fat  women  at  the  meno-pause, 
when  fatty  changes  may  be  suspected  ;  and  in  young  males, 
in  whom  long  continued  palpitation  sometimes,  I  believe, 
produces  temporary  hypertrophy  and  dilatation,  the  diagnosis 
may  be  especially  difficult.  In  the  latter  case,  provided  that 
the  valvular  apparatus  is  healthy,  that  there  is  no  disease  of 
the  kidneys,  that  there  is  no  evidence  of  adherent  pericardium, 
in  short,  no  obvious  mechanical  cause  of  enlargement,  we 
may,  I  think,  reasonably  conclude  that  the  enlargement  of 
the  heart  is  the  direct  result  of  the  palpitation,  and  that  when 
the  palpitation  has  subsided,  it  will,  in  all  probability,  dis- 
appear. 

2.  The  pJienoviena  of  the  attack. — In  neurotic  palpitation 
the  subjective  phenomena  are  out  of  all  proportion  to  the 
mechanical  derangement  of  the  circulation,  and  there  is  no 
evidence  of  any  structural  lesion  of  the  heart.  In  those  cases 
in  which  the  palpitation  is  associated  with  organic  disease  of 
the  heart,  symptoms  due  to  mechanicak  derangement  of  the 
circulation  are,  as  a  rule,  prominent. 

3.  The  effect  of  exertion  on  the  Jieart. — In  the  purely  neurotic 
forms  of  palpitation,  exertion  produces  little  or  no  short- 
ness of  breath  ;  whereas  in  the  organic  forms,  exertion  does 
produce  shortness  of  breath  and  excites  the  palpitation.  (In 
exophthalmic  goitre  and  anaemia,  shortness  of  breath  and 
palpitation  are  induced  by  exertion.) 

4.  The  age,  sex,  and  general  condition  of  the  patient. — Both 
neurotic  and  organic  palpitation  may,  of  course,  occur  at  any 
age  ;  but  neurotic  palpitation  is  most  common  in  young  adults, 
whereas  organic  palpitation  is  most  frequently  observed 
after  middle  life.  Neurotic  palpitation  is  most  common  in 
females  and  in  nervous  males  ;  organic  palpitation  occurs  in 
both  sexes,  and  in  persons  of  all  temperaments.  Palpitation 
in  an  old  person  is  always  suggestive  of  organic  disease.  In 
women  at  the  meno-pause,   severe    functional  palpitation  is 


666  Diseases  of  tJie  Heart. 

frequently  observed.  Middle-aged  men  who  are  depressed 
by  business  cares,  or  other  causes  of  mental  worry,  often 
suffer  from  palpitation  of  the  heart. 

5.  The  exciting  cause  of  the  attack. — Neurotic  palpitation 
is  generally  due  to  a  start,  fright,  emotional  disturbance  or 
reflex  impression  arising  in  some  of  the  peripheral  organs  ; 
whereas  organic  palpitation  is  most  frequently  occasioned 
by  muscular  effort  or  other  cause  of  increased  arterial  blood 
pressure.  In  anaemic  cases,  in  which  the  nerves  and  muscular 
fibres  of  the  heart  are  unduly  irritable  and  the  cardiac  walls 
at  the  same  time  degenerated,  an  attack  of  palpitation  may 
be  induced  in  both  ways,  i.e  through  the  nervous  system 
by  emotional  or  other  sudden  stimulation,  or  mechanically 
by  an  increased  strain  being  thrown  on  the  heart. 

Step  No.  2. — If  the  palpitation  is  associated  luith  organic 
disease  of  the  heart,  what  is  the  exact  nature  of  the  cardiac 
lesion  ? 

To  this  point,  which  must  of  course  be  determined  by  a 
careful  and  accurate  investigation  into  all  the  facts  of  the  case 
(the  symptoms  and  physical  signs),  I  need  not  further  refer 
here.  The  physician  must  of  course  remember  that  the 
structural  lesion  of  the  heart  may  be  either  primary  or 
secondary,  and  that  the  increased  arterial  blood  pressure, 
which  in  so  many  cases  is  the  direct  exciting  cause  of  the 
attack,  is  often  due  to  extra-cardiac  conditions.  It  is  par- 
ticularly important  in  all  cases  in  which  palpitation  is 
associated  with  hypertrophy  of  the  left  ventricle,  and  in 
which  the  hypertrophy  is  not  due  to  valvular  disease,  to 
examine  the  condition  of  the  urine.  Palpitation  is  in  fact 
a  very  common  symptom  in  the  later  stages  of  chronic 
Bright's  disease,  more  especially  of  the  cirrhotic  form. 

Step  No.  3. — If  there  is  no  organic  disease  of  the  heart, 
what  is  the  cause  of  the  attack  ? 

In  some  cases  this  question  is  easily  answered,  in  others  it 
can  only  be  determined  after  a  patient  and  careful  investiga- 
tion into  the  patient's  habits  and  mode  of  life. 

When  the  symptoms  and  signs  of  anaemia,  more  especially 
of  cardiac  anaemia  (pallor  of  the  mucous  membranes,  venous 


Diagnosis  of  Neurotic  Palpitation.  667 

hum  in  the  neck,  systoHc  pulmonary  murmur,  etc.)  are  present, 
a  sufficient  cause  for  the  palpitation  has  been  ascertained. 

The  condition  of  the  thyroid  and  of  the  eyeballs  should 
be  carefully  investigated,  for  palpitation  is  a  most  severe 
and  troublesome  symptom  in  exophthalmic  goitre.  It  is 
important  to  remember,  that  the  case  may  be  one  of  exoph- 
thalmic goitre  even  although  the  eyeballs  are  not  prominent, 
nor  the  thyroid  enlarged.  In  typical  cases  of  Grave's  disease 
(exophthalmic  goitre)  all  three  symptoms  (enlargement  of 
the  thyroid,  prominence  of  the  eyeballs,  and  excessive  action 
of  the  heart)  are  present,  but  it  is  not  very  uncommon  to 
find  the  prominence  of  the  eyeballs  wanting;  probably  in 
some  cases  the  thyroid  is  not  enlarged  ;  and  I  have  lately 
seen,  in  consultation,  a  gentleman  whom  a  distinguished 
London  physician  thinks  is  suffering  from  Grave's  disease,  in 
whom  the  enlargement  of  the  thyroid  and  the  prominence  of 
the  eyeballs  are  both  wanting,  but  in  whom  the  cardiac 
.symptoms  are  very  prominent. 

When  the  patient  is  not  anaemic,  and  when  the  eyeballs 
are  not  prominent,  and  the  thyroid  not  enlarged,  the  other 
possible  causes  of  palpitation  must  be  looked  for. 

In  all  cases,  more  especially  in  those  in  which  the  general 
health  is  below /^r,  the  apices  of  the  lungs  should  be  care- 
fully examined,  for  palpitation  is  not  uncommon  in  the  earlier 
stages  of  phthisis. 

In  young  women  when  there  is  no  obvious  cause,  the 
probability  that  the  palpitation  is  '  hysterical '  must  be  kept  in 
view,  and  other  indications  of  hysteria  inquired  after.  In 
young  males  the  frequency  with  which  palpitation  is  due  to 
sexual  excesses  and  irregularities,  and  to  over-indulgence  in 
tobacco,  must  be  borne  in  mind. 

When  the  palpitation  cannot  be  ascribed  to  any  of  the 
above-mentioned  causes,  the  fact  that  it  is  often  due  to  over 
indulgence  in  tea,  to  dyspepsia,  to  gout,  and  that  it  is  some- 
times caused  by  displacement  of  the  uterus,  ovarian  irritation, 
worms  in  the  intestine  or  other  form  of  peripheral  irritation 
must  be  remembered.  The  habits,  dietary  and  mode  of  life  of 
the  patient  must  be  carefully  inquired  into,  and  the  condition 


668  Diseases  of  the  Heart. 

of  the  different  organs  which  arc  Hkcly  to  produce  peripheral 
irritation  investigated. 

It  must  never  be  forgotten  that  mental  anxiety,  business 
worries,  monetary  cares,  love  disappointments,  and  the  like, 
are  very  often  at  the  root  of  the  whole  matter.  The  patient 
and  his  friends  must  therefore  be  discreetly  questioned  as  to 
the  existence  of  mental  worry. 

Prognosis. — The  prognosis  entirely  depends  upon  the 
cause,  and  the  facility  with  which  that  cause  can  be  removed. 
Speaking  generally,  the  prognosis  is  highly  favourable  in  cases 
of  pure  neurotic  palpitation.  There  are,  however,  some  ex- 
ceptions, exophthalmic  goitre,  for  example,  is  an  extremely 
intractable  disease,  and  the  palpitation  due  to  that  cause, 
though  it  can  in  many  cases  be  relieved  by  appropriate  treat- 
ment, is  seldom  completely  cured.  It  is  unnecessary,  however, 
to  go  into  details.  I  repeat,  that  the  prognosis  both  in  the 
organic  and  neurotic  forms  of  palpitation  must  be  entirely  based 
upon  the  exact  cause  of  the  condition,  and  the  possibility  of 
removing  that  cause  in  each  individual  case.  Palpitation  is, 
in  fact,  one  of  the  very  best  illustrations  which  can  be  given  of 
the  importance  of  a  full  and  exact  diagnosis.  The  prognosis 
and  treatment  of  palpitation  of  the  heart  are  mere  guess  work 
unless  the  exact  cause  of  the  condition  has  been  ascertained. 

Treatment. — T^xq  first  object  of  treatment  is  to  relieve  the 
paroxysm.  The  second,  to  remove  the  cause  and  prevent  the 
recurrence  of  the  attack. 

TJie  relief  of  the  paroxysm. — The  external  application  of 
cold  in  the  form  of  an  ice  bag  to  the  praecordial  region  ;  the 
administration  of  stimulants  (brandy,  ammonia,  ether)  by  the 
mouth  ;  the  inhalation  of  a  few  whifs  of  chloroform  ;  the 
subcutaneous  injection  of  morphia ;  the  administration  of  a 
full  dose  of  bromide  of  potassium  or  of  chloral ;  and  the 
application  of  a  galvanic  or  faradic  current  to  the  vagus  in 
the  neck,  are  the  chief  means  which  are  likely  to  prove 
efficacious  for  the  relief  of  the  paroxysm  itself.  The  attack  is 
sometimes  relieved  by  making  the  patient  take  a  few  deep 


Treatment  of  N^ciirotie  Palpitation.  669 

breaths,  or  by  applying  smelling  salts,  pepper,  etc.,  to  the 
nostrils,  by  anything  in  fact  which  produces  reflex  stimu- 
lation of  the  vagus.  Valerian,  assafoetida,  and  musk,  are 
useful  in  some  hysterical  cases.  When  the  palpitation  is 
due  to  mental  causes,  the  agitation  must  be  soothed,  calmed, 
and  allayed,  by  judicious  sympathy,  counsel,  or  commands,  in 
accordance  with  the  individual  peculiarities  of  the  patient. 
In  those  cases  (they  are  usually  organic)  in  which  the  palpita- 
tion is  due  to  a  sudden  increase  of  the  arterial  tension,  the 
inhalation  of  nitrite  of  amyl  is  the  most  rapid  and  satisfactory 
means  of  obtaining  relief ;  but  this  point  will  be  more  parti- 
cularly referred  to  under  the  treatment  of  angina  pectoris. 

TJie  prevention  of  the  recurrence  of  t/ie  attack. — The  first 
indication  is,  of  course,  to  remove  the  cause.  In  organic  cases 
this  is  for  the  most  part  impossible,  but  in  many  cases  of  neurotic 
palpitation  it  can  be  accomplished.  The  general  health  must 
be  raised  to  the  highest  possible  state  of  efficiency  ;  all  sources 
of  mental  anxiety  must,  if  possible,  be  removed  ;  the  patient 
should  lead  a  regular,  and,  as  far  as  possible,  outdoor  life, 
keeping  early  hours,  and  avoiding  excesses  of  all  kinds  ; 
arsenic,  and  iron  should  be  prescribed  if  there  is  any  anaemia  ; 
a  belladonna  plaster  over  the  praecordia  often  seems  to  be 
beneficial ;  bromide  of  potassium,  digitalis,  iron,  arsenic,  and 
strychnine  are,  in  my  experience,  the  most  useful  drugs. 
When  the  palpitation  is  clearly  neurotic,  the  patient  should  be 
distinctly  told  that  the  heart  is  not  diseased,  and  that  there  is 
no  fear  of  sudden  or  immediate  death.  The  application  of  a 
galvanic  or  faradic  current  to  the  vagus  and  sympathetic 
nerves  in  the  neck  is  often  distinctly  beneficial.  In  hysterical 
cases,  drug  treatment  is  of  minor  importance  compared  to  the 
general  management  of  the  case.  The  treatment  of  organic 
palpitation  need  not  be  specially  considered,  for  it  has  been 
already  described  under  the  different  organic  cardiac  lesions. 
(See  mitral  regurgitation,  cardiac  dilatation,  etc.) 


670  Diseases  of  tJic  Heart. 

IRREGULARITY  AND   INTERiMITTENT   ACTION. 

Irregular  and  intermittent  action  of  the  heart  are  often 
associated  with  palpitation,  but  frequently  occur  independ- 
ently of  that  condition.  Like  palpitation,  they  are,  in  some 
cases,  associated  with  organic  disease  ;  in  others  purely  func- 
tional and  neurotic. 

Organic  irregularity . — In  many  cases  in  which  the  heart 
is  diseased,  but  in  which  the  lesion  is  stationary,  and  the 
symptoms  slight  or  absent,  the  pulse  intermits  occasionally, 
and  is  irregular.  Slight  alterations  of  rhythm  may  be  of 
little  importance,  and  are  very  frequently  observed  in  old 
people  whose  arteries  are  atheromatous  and  whose  hearts  are 
somewhat  cirrhotic. 

Irregular  action  of  a  more  pronounced  and  serious  de- 
scription is  very  common  in  the  advanced  stages  of  mitral 
stenosis,  and  is  also  met  with  in  the  later  stages  of  mitral 
regurgitation.  It  is  of  frequent  occurrence  in  the  advanced 
stages  of  all  those  affections  in  which  the  cardiac  muscle  is 
degenerated,  and  is  observed  therefore  in  many  cases  of  peri- 
carditis, myocarditis,  fatty  and  fibroid  degeneration  ;  it  is  very 
common  in  dilatation,  and,  in  fact,  in  all  those  conditions  in 
which  compensation  is  failing  or  has  given  way.  It*  is  un- 
necessary to  describe  in  detail  the  various  forms  of  irregularity 
which  are  met  with  ;  the  most  serious  is  that  in  which  some 
of  the  ventricular  contractions  are  so  feeble  that  the  blood- 
wave,  which  is  propelled  into  the  aorta,  fails  to  reach  the 
wrist. 

Neurotic  irregularity. — Many  of  the  conditions  which  pro- 
duce palpitation  also  produce  neurotic  irregularity  of  the 
heart,  more  especially  over-indulgence  in  tea  and  tobacco, 
sexual  excesses,  and  gout. 

Symptoms  and pJiysical sigus. — Organic  irregularity  is  often 
unobserved  by  the  patient.  Neurotic  irregularity  and  inter- 
mission are  often  very  vividly  experienced,  the  heart  seeming 


Irregularity  and  Intermittent  Action.  671 

to  'stand  still,'  'turn  over,'  etc.,  a  feeling  of  palpitation  being 
often  at  the  same  time  experienced.  In  organic  cases,  the 
physical  signs  vary,  of  course,  with  the  nature  of  the  cardiac 
lesion.  In  purely  neurotic  cases,  the  intermittent  or  irregular 
action  of  the  heart  is  the  only  evidence  of  cardiac  derange- 
ment. 

Diagnosis. — The  steps  in  the  diagnosis  of  intermittent  or 
irregular  action  of  the  heart  are  the  same  as  in  the  case  of 
palpitation.  We  must  first  endeavour  to  determine  whether 
the  disordered  action  is  due  to  or  associated  with  structural 
organic  disease  of  the  heart.  The  condition  of  the  valvular 
apparatus  must  be  carefully  investigated,  and  it  is  important 
to  remember  that  in  many  cases  of  advanced  stenosis  of  the 
mitral  valve  in  which  the  cardiac  action  is  extremely  irregular, 
there  is  no  presystolic  murmur.^  The  presence  or  absence  of 
cardiac  dilatation  must  be  specially  noted,  and  the  exact 
condition  of  the  cardiac  muscle,  so  far  as  is  possible,  ascer- 
tained. I  must  again  emphasise  the  difficulty  of  diagnosing 
myocarditis,  fibroid  degeneration  and  fatty  heart,  and  insist 
upon  the  necessity  of  repeated  examinations  before  giving  a 
positive  opinion  in  cases  of  this  description.  After  having 
made  a  minute  physical  examination  of  the  heart,  the  effects 
of  exercise  should  be  noted,  the  presence  or  absence  of  other 
indications  of  cardiac  derangement  or  disease  ascertained,  in 
short,  all  the  other  points  to  which  I  have  referred  in  speaking 
of  the  diagnosis  of  palpitation  investigated. 

Prognosis.  —  The  prognosis  depends,  as  in  the  case  of 
palpitation,  upon  the  exact  cause  of  the  condition.  Intermis- 
sion or  simple  nervous  halt  is,  as  a  rule,  of  much  less  import- 
ance than  irregularity.  Each  case  must,  however,  be  judged 
on  its  own  merits,  special  attention  being  given  to  the  con- 
dition of  the  heart  and  the  exact  cause  of  the  cardiac  derange- 
ment, and  whether  that  cause  is  removable  or  not. 


'  The  reader  is  referred   to   the   description   of  mitral  stenosis,    its    physical 
signs  and  diagnosis  (see  page  477),  where  these  points  are  fully  treated  of. 


672  Diseases  of  the  Heart. 

Treatment. — The  treatment  of  organic  irregularity  must 
be  conducted  in  accordance  with  the  nature  of  the  cardiac 
lesion.  In  neurotic  cases  the  same  treatment  which  has  been 
recommended  for  the  treatment  of  neurotic  palpitation  is  to 
be  employed. 

ANGINA   PECTORIS. 

Definition. — A  neurotic  affection  characterised  by  par- 
oxysms of  intense  pain  in  the  region  of  the  heart,  and  a 
terrible  sensation  of  impending  death.  The  pain  usually 
radiates  through  the  thorax,  up  to  the  left  shoulder  and  down 
the  left  arm.  The  affection  is  in  many  cases  associated  with 
organic  disease  of  the  heart  and  the  root  of  the  aorta  ;  and 
in  its  typical  and  severe  forms  is  apt  to  prove  suddenly  fatal. 

yEtiology  and  Pathology. — The  group  of  symptoms,  in- 
cluded under  the  term  angina  pectoris,  may  in  all  probability 
be  produced  by  a  number  of  different  causes.  It  is  therefore 
difficult  to  give  a  satisfactory  systematic  account  of  the 
aetiology  and  pathology  of  the  condition  ;  and  it  is,  I  believe, 
impossible  to  advance  any  single  theory  which  will  satis- 
factorily account  for  the  phenomena  of  all  cases.  The 
essential  feature  of  angina  pectoris  is  pain  in  the  region  of  the 
heart,  in  fact  all  observers  are  agreed  in  thinking  that  the 
cardiac  pain  must  be  referred  to  the  area  of  distribution  of 
the  sensory  cardiac  nerves,  i.e.  to  the  heart  itself. 

Now  all  degrees  of  cardiac  pain  are  met  with, — but  it  is 
customary  to  limit  the  term  angina  pectoris  to  those  cases — 
rarely  met  with  before  the  age  of  forty — in  which  the  pain  is 
intense,  and  in  which  the  terrible  sensation  of  impending 
death  is  experienced  ;  while  those  cases  of  cardiac  pain,  which 
are  of  frequent  occurrence  in  young  persons,  and  in  which  the 
pain  is  usually  less  severe,  are  generally  included  under  the 
terra  pseudo-angina .  The  former  variety,  which  very  frequentl}- 
proves  fatal,  is  very  often  associated  with  coarse  pathological 
changes  in  the  heart  and  root  of  the  aorta,  and  very  generally, 
I  believe,  with  minute  structural  changes,  usually  degenerative 
in  character,  in  the  heart  or  blood-vessels.     The  latter  seldom, 


Pathology  of  Angina  Pectoris.  6^2^ 

if  ever,  proves  fatal,  and  is  rarely  associated  with  structural 
changes  in  the  heart  or  vascular  apparatus.  The  former  may  be 
appropriately  termed  the  organic  and  the  latter  'Ccvo.  functional 
form  of  angina  pectoris.  This  division,  into  a  serious  and 
organic  form  and  a  comparatively  trivial  and  inorganic  form 
of  the  disease,  is  of  practical  clinical  utility,  and  may  be  safely 
adopted,  provided  that  it  is  clearly  understood,  that  the  two 
forms  run  one  into  the  other,  and  that  it  is  sometimes  difficult 
or  impossible  to  separate  them  at  the  bedside.  It  must  also 
be  remembered  that  the  functional  form  of  angina  pectoris 
may,  and  I  believe  not  unfrequently  does,  occur  in  later  life, 
while  the  organic  form  is  occasionally,  though  it  must  be  con- 
fessed very  rarely,  met  with  before  the  age  of  forty.  In  order 
to  understand  the  phenomena  of  angina  pectoris,  so  far  as  our 
imperfect  knowledge  will  at  present  allow,  it  will  be  well 
perhaps  to  consider  cardiac  pain  as  a  whole,  and  to  refer 
briefly  to  the  construction,  so  to  speak,  of  the  sensory  nerve 
apparatus  of  the  heart. 

In  conditions  of  health,  and  when  the  heart  is  contracting 
quietly,  we  are  unaware  of  the  action  of  the  organ.  It  is  only, 
in  fact,  when  the  cardiac  action  is  markedly  deranged,  either 
as  the  result  of  temporary  and  functional,  or  permanent  and 
organic  causes,  that  we  are  conscious  of  any  cardiac  sensations. 

We  become  conscious  of  the  cardiac  action  when  the  sen- 
sory nerve  terminations  in  the  heart  and  adjacent  structures  are 
more  powerfully  stimulated  than  they  are  in  normal  tranquil 
action  of  the  organ  ;  under  such  circumstances  an  impression  is 
conducted  to,  and  registered  by,  the  sensory  perceptive  centres 
in  the  cerebrum. 

The  exact  course  of  the  sensory  nerve  fibres,  which  con- 
vey impressions  from  the  heart  to  the  cerebrum,  has  not  yet 
been  definitely  determined.  In  some  of  the  lower  animals, 
the  frog,  for  example,  sensory  impressions  seem  to  be  con- 
ducted upwards  by  a  special  branch  of  the  vagus,  which  has, 
therefore,  been  termed  the  sensitive  nerve  of  the  heart ;  but 
it  is  probable  that  in  man  the  channels  of  sensory  conduction 
are  by  no  means  so  limited  ;  the  phenomena  of  angina 
pectoris  seem,  in  fact,  to  prove  that  the  cardiac  branches  of 

U   U 


674  Diseases  of  the  HearL 

the  sympathetic  contain  sensory  fibres.  In  man,  sensory 
impressions  are  carried  from  the  heart  by  the  sympathetic 
fibres  connected  with  the  cardiac  plexus,  possibly  also,  as  in 
the  frog,  by  the  cardiac  branches  of  the  vagus. 

The  sympathetic  branches  of  the  cardiac  plexus  pass,  it 
will  be  remembered,  to  the  first  dorsal  and  three  cervical 
"■an<5-lia  and  thence  to  the  spinal  cord.  Sensory  impressions, 
passing  to  the  cerebrum  from  the  heart  through  the  sym- 
pathetic, pass  via  the  spinal  cord,  while  sensory  impressions 
passing  from  the  heart  through  the  vagus  join  the  nerve 
centres  at  the  medulla  oblongata. 

The  exact  course  of  the  sympathetic  fibres,  which  are  sup- 
posed to  conduct  cardiac  impressions  upwards,  in  the  spinal 
cord  is  unknown.  The  exact  position,  too,  of  the  perceptive 
cerebral  centre  which  receives  such  impressions  is  undeter- 
mined. 

Now  cardiac  pain,  i.e.  pain  referred  to  the  heart  itself  ma\- 
theoretically  result  from  excessive  stimulation  of  any  part 
of  the  sensory  nerve  apparatus  connected  with  the  heart.' 
Theoretically,  therefore,  we  may  suppose  that  cardiac  pain 
may  be  due  to  : — 

(i)  Irritation  of  the  sensory  nerve  terminations  in  the 
wall  of  the  heart  itself,  the  sensory  parts  of  the  coronary 
plexus  (sensory  ganglia,  if  there  are  sensory  ganglia,  and 
sensory  branches.) 

(2)  The  sensory  nerve  fibres  composing  the  cardiac 
plexus. 

(3)  The  sensory  conductors  which  connect  the  cardiac 
plexus  with  the  sensory  perceptive  centres  in  the  cerebrum. 
(In  the  case  of  the  sympathetic  conductors,  the  seat  of  irrita- 
tion might  theoretically  be  placed  in  {a)  the  branches  connect- 
ing the  cardiac  plexus  with  the  three  cervical  and  first  dorsal 
ganglia,  {b)  these  ganglia  themselves,  {c)  the  branches  con- 
necting the  ganglia  with  the  spinal  cord,  {d)  the  spinal  cord 

'  When  a  sensory  nerve  or  sensory  centre  is  irritated,  the  pain  which  resuhs  is 
referred  in  accordance  with  the  law  of  '  eccentric  projection '  to  that  part  of  the 
periphery  from  which  the  sensory  conductors  or  sensory  centres  are  in  the  habit 
of  receiving  impressions,  rather  than  to  the  point  of  irritation  itself. 


Pathology  of  Angina  Pectoris.  675 

itself,  {/)  the  conductors  above  the  spinal  cord,  i.e.  between 
the  spinal  cord  and  the  perceptive  centre.) 

(4)  The  perceptive  cerebral  centres  themselves. 

It  is  probable,  I  think,  that  cardiac  pain  is  actually  pro- 
duced in  most  of  these  ways.  But  before  proceeding  to  con- 
sider the  exact  manner  in  which  the  pain  of  angina  pectoris 
is  produced,  let  us  turn  for  a  moment  to  the  records  of  post- 
mortem examinations,  and  see  what  lesions  have  been  actually 
found  after  death.  In  a  large  proportion  of  typical  cases  of 
true  angina  pectoris  (the  form  which  I  term  organic,  and 
which  is  apt  to  prove  suddenly  fatal),  the  coronary  arteries 
have  been  found  ossified.  It  is  obvious  that  this  condition  is 
not  of  itself  the  cause  of  the  angina,  for  ossification  of  the 
coronary  arteries  is  an  extremely  common  condition,  and  it  is 
only  in  a  small  minority  of  the  cases  that  symptoms  of  angina 
are  observed. 

Possibly  in  those  cases  in  which  angina  pectoris  does 
occur,  the  coronary  nerves  (which  are  so  closely  connected,  in 
their  course  over  the  exterior  of  the  heart  with  the  branches 
of  the  coronary  arteries)  are  implicated,  just  as  the  cardiac 
nerves  which  ramify  over  the  arch  of  the  aorta  are  affected  in 
some  cases  of  atheroma  and  chronic  arteritis  of  the  base  of 
the  aorta  ;  but  to  this  point  I  will  again  presently  refer. 

In  many  cases,  the  heart  muscle  is  fatty  or  otherwise  de- 
generated. In  a  considerable  proportion  of  the  cases  of  angina 
pectoris  the  base  of  the  aorta  is  dilated  or  aneurismal ;  in 
some  cases  pericarditis  has  been  observed  ;  and  in  three  cases 
which  have  been  carefully  examined  by  Lancercaux  Peter, 
and  Bazy,  a  distinct  change  has  been  found  in  the  branches 
of  the  cardiac  plexus  passing  over  the  root  of  the  aorta. 
Peter,  for  example,  found  in  one  of  his  cases  slight  dilatation 
of  the  base  of  the  aorta,  increased  vascularity  and  thickening 
of  the  aortic  coats,  and  evidence  of  old  pericarditis  at  the  base 
of  the  heart.  The  branches  of  the  cardiac  plexus,  which  were 
carefully  dissected  out  from  the  fibrous  adhesions  surrounding 
the  root  of  the  aorta,  were  found  on  microscopical  examination 
to  be  in  a  condition  of  chronic  inflammation,  the  nerve  tubes 
were    separated    by  masses   of   connective  tissue   containing 


676  Diseases  of  the  Heart. 

numerous  nuclei  ;  some  of  the  nerve  tubes  were  strangled,  as 
it  were,  by  this  fibrous  tissue,  their  myeline  sheaths  ruptured 
and  transformed  into  an  amorphous  fatty  mass.^ 

In  some  cases,  the  cardiac  valves  (and  more  especially  the 
aortic  valves)  have  been  diseased,  in  fact,  all  forms  of  cardiac 
lesion  have  been  found.  Very  frequently  the  peripheral  blood- 
vessels, as  well  as  the  aorta,  are  atheromatous.  In  some  cases, 
the  heart  has  been  said  to  be  healthy,  but  structural  changes 
are,  I  believe,  present,  either  in  the  heart  or  the  arteries,  or 
in  both,  in  the  vast  majority,  if  not  in  all  cases  of  angina 
pectoris  which  prove  fatal. 

Let  us  now  endeavour  to  determine  the  exact  manner  in 
which  the  pain  is  produced  in  cases  of  angina  pectoris.  In 
most  cases  it  is,  I  believe,  due  to  irritation  of  the  sensory 
nerve  terminations  in  the  wall  of  the  heart  itself.  The  exact 
manner  in  which  the  cardiac  nerve  terminations  are  irritated, 
has  not  yet  been  definitely  determined.  A  very  plausible 
theory  is  that  which  supposes  that  the  irritation  is  due  to 
spasmodic  contraction  of  the  cardiac  muscle  ;  that  the  cardiac 
pain  is  in  fact  similar  to  the  violent  pain  which  is  experienced 
in  the  calf  muscles  when  they  are  spasmodically  contracted 
as  in  ordinary  cramp.  Further,  we  know,  as  the  result  of 
actual  experience,  that  cramp  in  the  calf  is  mo.st  apt  to  arise 
when  the  muscle  is  exhausted  and  fatigued — all  football 
players  must  be  well  aware  of  this  fact.  Further,  Gaskell's 
observations  have  shown  that  when  the  vitality  of  the  cardiac 
muscle  is  impaired  by  exhaustion,  by  injury,  by  malnutri- 
tion, the  cardiac  muscle  loses  its  power  of  rapid  contraction, 
and  contracts  with  a  prolonged  tonic  contraction  in  the  same 
way  as  unstriped  muscle.  Again,  clinical  experience  has 
shown  that  during  the  paroxysm  of  angina  pectoris  the 
systemic  arterial  tension  is,  in  many  cases,  very  notably 
increased. 

Possibly,  too,  in  those  cases  of  angina  pectoris  in  which 
the  coronary  arteries  are  atheromatous,  the  degenerative 
process  which  commenced  in  the  inner  coat  of  the  coronary 
arteries  (endarteritis  deformans)  has   extended   to  the  outer 

'   7 raitc  cliniquc  ct  pratique  dcs  maladies  du  Ca'iir,  p.  673. 


Pathology  of  Angina  Pectoris.  677 

coat  and  implicated  the  coronary  nerves.  Under  such  cir- 
cumstances the  terminal  nerve  fibres  in  the  cardiac  walls 
would,  we  may  theoretically  suppose,  be  in  an  unusually 
irritable  condition. 

Now,  taking  all  these  facts  in  connection,  we  may,  I 
think,  with  some  probability  theorise  that  in  many  cases  of 
angina  pectoris  the  sequence  of  events  is  as  follows  : — 

Firstly,  the  blood  pressure  in  systemic  arterial  circulation 
is  suddenly  increased,  either  as  the  result  of  changes  arising 
in  the  central  nervous  system  (vaso-motor  centre),  or  in  con- 
sequence of  some  external  condition  (sudden  effort,  exposure 
to  cold,  mental  agitation,  etc.),  or  reflex  impulse  arising  within 
the  body. 

Secondly,  in  consequence  of  the  sudden  increase  in  the 
peripheral  resistance,  the  left  ventricle,  or  rather  those  fibres 
of  the  left  ventricle,  which  are  degenerated  either  as  the  result 
of  imperfect  blood  supply  (disease  of  the  coronary  arteries) 
or  of  degenerative  changes  in  the  cardiac  muscle,  are  thrown 
into  a  temporary  condition  of  spasm  or  cramp,  which  is 
attended  with  severe  pain.  It  is  of  course  quite  possible, 
indeed  probable,  that  in  some  cases  in  which  the  cardiac 
nerves  are  diseased,  the  attack  arises  independently  of  any 
sudden  increase  of  the  peripheral  resistance.  Should  the 
supposition,  which  has  previously  been  adduced  as  to  the 
possibility  of  a  lesion  of  the  terminal  branches  of  the  coronary 
nerves,  be  correct, — powerful  spasmodic  contraction  of  the 
left  ventricle  not  amounting  to  cardiac  cramp,  and  which 
under  ordinary  circumstances  would  not  be  attended  with 
cardiac  pain,  might  possibly  be  sufficient  to  produce  the 
condition. 

Tliirdly,  this  irritation  of  the  terminal  branches  of  the 
cardiac  nerves,  is  reflected,  via  the  sympathetic  branches  of 
the  cardiac  plexus  and  the  spinal  cord,  to  other  parts  of  the 
periphery.  Dr  Allen  Sturge,  in  a  very  suggestive  paper,  to 
which  I  am  much  indebted,  and  to  which  I  would  refer  my 
readers  who  are  interested  in'  this  subject,  states,  'that  it  is 
only  when  the  commotion  has  begun  in  the  cord,  or  passed 
up  to  the  grey  matter  of  the  spinal  cord  from  the  sympathetic, 


678  Diseases  of  the  Heart. 

that  any  great  extension  (such  as  radiation  to  the  arm  or  wall 
of  the  chest)  can  take  place.' ^ 

Wc  would  naturally,  of  course,  expect  that  the  reflex 
impression  would  be  first  conducted  to  those  parts  of  the 
periphery,  which  are  more  immediately  connected  with  the 
spinal  centres  to  which  the  cardiac  branches  of  the  sym- 
[)athetic  pass,  and  that  when  the  irritation  was  very  extreme, 
the  impression  mi<^ht  extend  to  other  and  more  distant  masses 
of  spinal  grey  matter,  and  be  reflected  to  other  and  more 
distant  parts  of  the  periphery.  And  such  is  in  fact  the  case. 
In  cases  of  true  angina  pectoris  the  pain  radiates  through  the 
thorax,  up  to  the  left  shoulder,  and  down  the  left  arm,  some- 
times to  the  tips  of  the  fingers  ;  it  not  unfrequently  passes  up 
the  left  side  of  the  neck,  and  in  exceptionally  severe  cases  it 
may  pass  down  the  right  arm,  or  to  the  lower  extremities,  in 
fact  to  almost  all  parts  of  the  body.  The  radiation  to  the 
left  shoulder  and  left  arm  is  so  constantly  observed  in  tj-pical 
cases  of  angina  pectoris,  that  it  has  been  by  some  writers 
supposed  that  the  primary  lesion  is  situated  in  the  spinal  cord 
itself.-  Anstie,  for  example,  thought  that  angina  pectoris 
is  probably  due  to  'a  mainly  unilateral  morbid  condition  of 
the  lower  cervical  and  upper  dorsal  portion  of  the  cord, 
liable  of  course  to  be  seriously  aggravated  by  such  peripheral 
sources  of  irritation  as  would  be  furnished  by  diseases  of  the 
heart,  and  especially  b}'  diseases  of  the  coronary  arteries  ;' 
but  with  this  opinion  I  cannot  agree.  In  no  case,  so  far  as  I 
am  aware,  has  a  lesion  of  the  spinal  cord  been  found,  and  it 
is  extremely  difficult  to  believe  that  any  spinal  lesion  could 
be  so  constantly  unilateral  ;  the  very  fact,  in  short,  which 
Anstie  advanced  against  the  radiation  of  the  pain  outwards 
from  the  heart,  viz.  the  unilateral  character  of  the  brachial 
pain,  seems  to  me  strongly  opposed  to  his  view.  The 
unilateral  character  is,  I  believe,  due  to  the  fact  that  the 
irritation  of  the  cardiac  nerves  is  in  most  cases  limited  to  the 
nerves  of  the  left  ventricle,  for  it  is  this  cavity  which  has  to 
overcome  the  sudden  increase  in  the  peripheral  arterial  resist- 
ance which  is  often  the  starting  point  of  the  attack.     When 

'  Brain,  January  1883,  p.  496. 


PatJwlogy  of  Angina  Pe:toris.  679 

the  pain,  which  has  originated  in  the  region  of  the  heart,  and 
has  radiated  to  the  left  arm  in  the  usual  way,  passes,  as  it 
sometimes  does  (but  only  in  severe  or  exceptional  cases),  to 
the  right  arm,  the  peripheral  irritation  has  been  sufficiently 
severe  to  pass  over  to  the  opposite  side  of  the  spinal  cord. 
In  other  cases  the  radiation  of  the  pain  to  the  right  arm  is. 
I  think,  to  be  explained  either  by  supposing  that  some  of  the 
fibres  of  the  right  ventricle  have  also  become  affected,  and 
the  nerve  terminations  in  the  walls  of  that  cavity  have  become 
irritated  ;  or,  that  the  primary  seat  of  the  lesion  {i.e.  of  the 
irritation)  is  outside  the  heart  in  the  coronary  plexus, — a 
lesion,  for  example,  of  the  root  of  the  aorta. 

It  has  also  been  supposed  by  some  writers  that  the 
paroxysm  of  angina  pectoris  can  be  produced  by  a  sudden 
diminution  of  the  blood  supply  to  the  heart  itself,  the  coronary 
arteries  sharing  of  course  in  the  general  vascular  spasm  which 
is  the  cause  of  the  increased  arterial  tension  to  which  I  have 
previously  referred  as  the  exciting  cause  of  the  attack. 

In  other  cases  of  angina  pectoris  the  primary  lesion  is 
probably  extra-cardiac.  I  have  previously  stated  that  in 
many  cases  the  base  of  the  aorta  is  diseased,  and  that  in  some 
cases  of  this  description  an  actual  lesion  of  the  branches  of 
the  cardiac  plexus,  which  ramify  over  the  arch  of  the  aorta, 
has  been  demonstrated.  The  same  explanation,  i.e.  direct  irri- 
tation of  the  branches  of  the  cardiac  plexus,  would  of  course 
satisfactorily  account  for  the  occurrence  of  angina-like  pain 
in  cases  of  pericarditis.  (It  must,  of  course,  be  remembered 
that  in  those  cases  in  which  the  branches  of  the  cardiac 
plexus  are  involved  in  a  chronic  lesion,  the  degenerative 
changes  would  probably  extend  downwards  to  the  peripheral 
terminations  of  the  cardiac  nerves  in  the  heart,  and  that 
the  partially  degenerated  nerves  might  be  more  irritable 
than  in  health.  Under  such  circumstances,  cardiac  spasm, 
produced  in  the  manner  I  have  previously  endeavoured  to 
explain,  would  be  very  likely  to  cause  an  attack  of  angina 
pectoris.)  Possibly  too,  in  those  cases  in  which  a  lesion  of 
the  cardiac  nerves  surrounding  the  aorta  cannot  be  demon- 
strated, there  may  be  lesion  of  the  branches  of  the  coronary 


68o  Diseases  of  tJie  Heart. 

plexus,  or  degenerative  changes  in  the  coronary  arteries 
impHcating  the  coronary  nerves  which  ramify  so  extensively 
over  these  vessels.  Such  a  supposition  would  go  far  to 
explain  the  frequent  association  of  disease  of  the  coronary 
arteries  with  angina  pectoris. 

In  other  cases  of  angina  pectoris,  the  primary  lesion  is 
possibly  situated  in  the  nerve-centres.  This  is  probably,  I 
think,  the  cause  of  the  angina-like  attacks  which  are  some- 
times met  with  in  hysterical  women.  Under  this  head  also 
I  would  place  many  of  the  cases  of  so  called  pseudo-angina. 

Cases  of  functional  angina  pectoris,  or  pseudo-angina,  in 
which  there  is  no  structural  lesion  of  the  heart  or  other  parts 
of  the  vascular  apparatus,  might  very  appropriately  be  termed 
cases  of  cardiac  neuralgia.  Cases  of  pseudo-angina  are  of 
frequent  occurrence  in  anaemic  and  hysterical  women,  and  in 
young  males  who  are  exhausted  by  sexual  or  other  excesses, 
or  who  over  indulge  in  tobacco. 

The  organic  form  of  angina  pectoris  is  often  met  with 
in  gouty  subjects,  and  is  popularly  included  with  other  condi- 
tions under  the  term  '  gout  in  the  stomach.'  Gout,  it  will  be 
remembered,  is  one  of  the  conditions  which  produce  atherom.a, 
and  therefore  disease  of  the  aorta  and  coronary  arteries. 
In  short,  cardiac  neuralgia  is  produced  by  the  same  causes 
which  produce  neuralgia  in  other  parts  of  the  body.  Why 
the  neuralgia  affects  the  nerves  of  the  heart  it  is  usually 
impossible  to  surmise,  just  as  it  is  usually  impossible  to 
ascertain  what  are  the  causes  which  determine  the  locality  of 
the  lesion  in  neuralgia  of  the  fifth  nerve  for  example. 

Symptoms  and  Physical  Signs. — Angina  pectoris,  of  which 
it  will  be  only  necessary  to  describe  the  more  severe  forms,  is 
a  paroxysmal  affection,  and  is  seldom  observed  before  the 
age  of  forty.  The  patient  is  usually  a  male,  for  the  athero- 
matous condition  of  the  aorta  and  coronary  arteries,  which 
is  such  an  important  factor  in  the  production  of  the  organic 
form  of  the  disease,  is  comparatively  seldom  observed  until 
after  middle  life,  and  is  much  more  common  in  men  than 
in  women.     The  exciting  cause  of  the  paroxysm  is  in  many 


SyniptoDis  and  Physical  Signs  of  Angina  Pectoris.  68 1 

cases  bodily  exertion  (walking  too  quickly,  climbing  a  hill, 
etc.),  mental  excitement,  straining  at  stool,  exposure  to  cold, 
or  other  causes  of  increased  arterial  blood  pressure.  In 
some  cases  no  definite  exciting  cause  can  be  ascertained. 
The  attack  commences  with  pain  in  the  region  of  the  heart ; 
in  well  marked  cases  the  pain  is  intense,  it  radiates  through 
the  thorax  to  the  spine,  and  usually  extends  up  to  the  left 
shoulder  and  down  the  inner  side  of  the  left  arm,  often  to 
the  tips  of  the  fingers.  It  also  radiates  up  the  left  side 
of  the  neck;  less  frequently  it  extends  to  the  right  shoulder 
and  down  the  right  arm;  and  in  exceptional  cases  it  has 
been  known  to  pass  to  the  lower  extremities,  and  seemed 
in  fact  to  shoot  all  over  the  body.  In  rare  cases  the  pain 
is  more  marked  in  the  right  arm  than  in  the  left ;  in  cases  of 
this  description,  and  indeed  in  most  cases  in  which  the  exten- 
sion is  to  the  right  as  well  as  to  the  left,  it  is  probable,  I 
think,  that  the  lesion  will  be  found  at  the  root  of  the  aorta,  or 
in  the  aortic  arch,  rather  than  in  the  heart  itself.  It  is  obvious, 
on  anatomical  grounds,  that  a  lesion  of  the  aorta  implicating 
the  branches  of  the  cardiac  plexus,  will  in  most  cases  involve 
the  branches  of  the  sympathetic  proceeding  from  the  right 
side  of  the  spinal  cord  as  well  as  those  passing  to  the  left. 
In  addition  to  this  intense  pain,  a  terrible  feeling  of  impending 
death  is  experienced  ;  in  many  cases  the  chest  feels  as  if 
it  were  fixed  in  a  vice,  the  patient  dreads  making  any  move- 
ment, and  does  not  dare  to  take  a  deep  breath  ;  the  counte- 
nance is  expressive  of  the  terrible  agony  and  dreadful  sensation 
of  impending  dissolution  which  the  patient  is  experiencing, 
the  features  are  generally  at  the  same  time  pinched,  the 
colour  pale,  and  the  face  in  some  cases  covered  with  a  cold 
clammy  perspiration;  in  short,  in  most  cases  the  features  are 
at  the  same  time  expressive  of  suffering,  fear,  and  collapse. 

The  condition  of  the  pulse  varies  in  different  cases  ;  usually 
it  is  small,  quick,  and  hard,  and  sphygmographic  observations 
have  shown  that  in  many  cases  the  arterial  blood  pressure  is 
very  markedly  increased.  In  some  cases  the  pulse  is  irregular. 
In  a  case  of  hysterical  angina  pectoris  which  was  under  my 
care  for  some  time,  the  patient  lay  for  some  days  in  a  state 


682  Diseases  of  tJie  Heai't. 

of  collapse,  in  which  the  skin  was  cool  and  pale,  and  the 
pulse  beating  at  the  rate  of  180-200  per  minute  ;  severe 
and  very  frequently  recurring  pain,  which  presented  all  the 
usual  characteristics  of  angina-like  pain,  was  experienced  in 
the  precordial  region  ;  the  pulse  tension  was  not  increased, 
and  these  attacks  were  not  relieved  by  the  nitrite  of  amyl. 
In  some  cases  the  action  of  the  heart  has  been  said  to  be 
natural  and  the  pulse  tranquil.  In  others  the  pulse  has  been 
found  to  be  slower  than  normal  during  the  attack. 

The  respirations  are  u.sually,  but  not  invariably  increased 
in  frequency;  as  a  rule  the  respiratory  movements  are  more 
superficial  and  more  shallow^  than  in  health,  but  in  some  cases 
dyspnoea  is  observed.  Vomiting  has  been  noted  in  some 
cases,  in  others  vertigo,  and  occasionally  more  serious  indica- 
tions of  derangement  of  the  cerebral  nerve  centres,  such  as 
spasmodic  twitchings,  or  even  general  epileptiform  convul- 
sions, occur. 

The  paroxysm  is  usually  of  short  duration  (a  few  minutes 
to  a  quarter  of  an  hour)  but  in  exceptional  cases  it  lasts  for  a 
longer  time.  As  the  attack  passes  off,  wind  is  frequently 
eructated  from  the  stomach,  and  in  some  cases  there  is  a 
copious  discharge  of  pale,  limpid  urine. 

After  a  severe  attack,  the  patient  is  naturally  much 
exhausted,  he  looks  terribly  shaken ;  for  days,  or  even  longer, 
his  whole  expression  and  bearing  may  be  indicative  of  the 
dreadful  nature  of  the  ordeal  which  he  has  just  passed  through. 
After  the  pain  subsides,  a  feeling  of  numbness  (anaesthesia), 
and  sometimes  of  loss  of  motor  power  (paresis)  is  experienced 
in  the  affected  arm,  i.e.  usually  the  left  arm.  Occasionally, 
too,  there  is  numbness  and  loss  of  sensibility  in  the  skin  of  the 
praecordia.  Sometimes  hypera^sthesia,  and  not  anaesthesia,  is 
observed. 

Should  the  physician  have  an  opportunity  of  examining 
the  heart  during  the  attack,  the  action  will,  as  a  rule,  be  found 
to  be  quickened,  and  the  impulse  and  sounds  weaker  and 
more  distant  than  in  health.  In  some  cases  the  action  of  the 
heart  has  been  said  to  be  quite  normal.  In  those  cases  in  which 
valvular    lesions,    pericarditis,    and    other    organic    changes. 


Symptoms  and  Physical  Signs  of  Angina  Pectoris.  683 

attended  with  well-marked  physical  signs  are  present,  the 
usual  indications  of  those  lesions  will  of  course  be  observed. 

After  a  sufficient  time  has  elapsed  to  allow  of  recovery 
from  the  exhaustion,  collapse,  and  after-effects  of  the  attack, 
—and  some  days  or  even  weeks  may  be  required  for  com- 
plete recovery  — the  patient  is  restored  to  his  previous  con- 
dition of  health.  It  is  very  essential  after  convalescence 
has  been  fairly  established,  to  make  a  minute  and  careful 
examination  of  the  heart  and  blood-vessels.  Special  atten- 
tion should  be  given  to  the  condition  of  the  heart  itself, 
the  base  of  the  aorta,  and  the  peripheral  arteries.  Evi- 
dence of  dilatation  of  the  root  of  the  aorta,  and  of  general 
atheroma — conditions  which  suggest  the  presence  of  athe- 
roma of  the  coronary  arteries — will,  in  many  cases,  be 
detected.  In  others,  the  usual  symptoms  and  signs  of  aortic 
regurgitation  will  be  observed  ;  and  in  a  {q.\n  cases  the  physical 
indications  of  fatty  heart.  In  many  cases,  the  heart  itself 
appears  to  be  healthy,  but  the  peripheral  blood-vessels  and 
the  condition  of  the  radial  pulse  are  suggestive  of  commencing 
arterial  degeneration  ;  the  arcus  senilis  is  not  infrequent 
in  such  cases,  and  though  /^r  se  of  little  value  as  a  diagnostic 
of  any  special  cardiac  lesion,  it  is  suggestive  of  degenerative 
changes  in  the  vascular  system.  In  some  cases,  more  especially 
in  gouty  subjects,  the  condition  of  the  urine  may  suggest 
cirrhotic  changes  in  the  kidney. 

In  pseudo-angina,  or  functional  angina  as  I  prefer  to 
term  it,  there  are  no  indications  of  cardiac,  aortic,  or  vascular 
disease.^ 

The  frequency  with  which  the  paroxysms  recur  varies 
considerably  in  different  cases.  Quite  exceptionally  there 
is  no  return  of  the  attack  ;  very  frequently,  several  months, 
it  may  even  be  years,  separate  the  first  and  second  attacks  ; 
the  interval  between  the  second  and  third  attacks  is  usually 
shorter  ;   and   in  most    cases    as    the    disease   goes    on,    the 

'  I  refer  of  course  to  typical  cases  of  pseudo-angina,  such  as  are  met  with  in 
young  males  and  hysterical  females,  and  do  not  include  the  prascordial  pains  {not 
amounting  to  true  angina  pectoris)  which  are  met  with  in  some  cardiac  affections 
— aortic  regurgitation  for  example. 


684  Diseases  of  tJie  Heart. 

paroxysms  become  more  and  more  frequent,  and  arc  more 
and  more  easily  excited.  Ultimately  the  slightest  exertion, 
such  as  stooping  to  put  on  boots,  may  produce  a  paroxysm. 
The  severity  of  the  attacks  too  is  apt  to  increase  as  the  case 
progresses. 

Diagnosis. — The  diagnosis  of  severe  cases  of  angina 
pectoris  does  not  present  any  difficulty,  the  character  of  the 
pain,  the  terrible  nature  of  the  suffering,  more  especially  the 
dread  feeling  of  impending  death,  are  quite  distinctive.  It 
is  very  important,  however,  to  remember,  firstly,  that  in 
grave  cases  of  angina  pectoris  the  pain  is  not  alwaj-s  typical 
and  severe ;  and  secondly,  that  severe  pain  in  the  region 
of  the  heart,  apparently  identical  with  the  pain  of  the  organic 
form  of  the  disease,  may  be  due  to  purely  functional  causes. 
When  the  attack  is  not  a  very  severe  one,  and  more  especially 
when  the  ph}'sician  has  not  had  an  opportunity  of  witnessing 
a  paroxysm,  it  may  be  extremely  difficult  to  form  an  opinion 
as  to  the  true  nature  of  the  case. 

Angina-like  pain  should,  however,  always  excite  grave 
apprehension,  and  in  all  cases,  in  which  such  pain  is  expe- 
rienced, the  physician  must  endeavour  to  determine  whether 
he  has  to  do  with  the  organic  or  the  functional  form  of  the 
disease.  In  attempting  to  decide  this  very  important  ques- 
tion, attention  should  be  directed  to  the  following  points  : — 

I.  Tlic  condition  of  tlie  licart  and  vascular  apparatus 
generally.  2.  The  age  and  sex  of  the  patient.  3.  The  severity 
and  character  of  the  symptoms. 

Organic  disease  of  the  heart,  more  especialh'  aortic  valvular 
disease;  simple  or  aneurismal  dilatation  of  the  aorta;  atheroma 
of  the  superficial  vessels  ;  the  presence  of  an  areiis  senilis, 
and  in  fact  any  other  indications  of  degenerative  changes, 
more  especially  of  degenerative  changes  likely  to  affect  the 
heart  and  blood-vessels  ;  the  facts  that  the  patient  is  over  forty 
years  of  age,  and  is  a  male,  that  the  pain  was  severe,  that  it 
radiated  down  the  left  arm,  and  that  the  attack  was  accom- 
panied by  the  feeling  of  impending  death,  are  all  strongly 
suggestive  of  the  organic  and  serious  form  of  the  disease. 


Prognosis  of  Angina  Pectoris.  685 

When  on  the  contrary  the  physician  is  satisfied  that  there 
is  no  disease  of  the  heart  or  blood-vessels,  when  the  patient 
is  a  female,  and  especially  when  in  addition  the  patient 
(whether  a  male  or  a  female)  is  under  forty  years  of  age,  and 
when  there  is  no  reason  to  suspect  degenerative  arterial 
changes,  the  diagnosis  of  functional  angina  pectoris  may  be 
ventured  upon. 

I  must,  however,  caution  the  obsei"\'er  against  too  hastily 
deciding  in  favour  of  the  functional  form  of  the  disease 
if  there  is  any  reason  to  suspect,  either  from  the  age  of  the 
patient,  or  any  other  fact,  that  degenerative  arterial  changes 
may  be  present.  It  must  never  be  forgotten  that  the  coronary 
arteries  may  be  atheromatous  in  cases  in  which  there  are  no 
physical  signs  of  cardiac  disease,  no  evidence  of  disease  of 
the  aorta,  and  even  in  which  there  is  no  distinctive  evidence 
of  atheroma  of  the  superficial  vessels.  It  must  also  be 
remembered  that  it  is  often  impossible  to  detect  a  small 
aneurism  at  the  root  of  the  aorta  ;  while,  as  we  have  previously 
seen,  the  diagnosis  of  fatty  heart — a  condition  which  may  be 
attended  with  angina  pectoris — is  often  most  difficult. 

Prognosis. — The  prognosis  of  the  organic  form  of  angina 
pectoris  is  most  grave,  and  it  must  never  be  forgotten  that 
the  patient  may  die  during  the  attack.  The  opinion  must  to 
a  large  extent  be  based  upon  the  condition  of  the  heart  and 
arteries,  the  frequency  and  severity  of  the  parox}-sms,  the 
circumstances  and  surroundings  of  the  patient,  his  capabilities 
of  following  out  the  treatment  which  is  recommended,  more 
especially  his  capabilities  of  avoiding  all  causes  of  sudden 
increased  arterial  strain,  his  mental  temperament,  etc.  It 
must  always  be  remembered  that  a  patient  who  has  once  had 
a  severe  and  typical  attack  of  angina  pectoris  may  at  any 
time  have  a  second,  which  may  prove  immediately  fatal.  The 
tendency  is,  in  fact,  to  the  more  frequent  recurrence  of  the 
attacks  as  the  case  progresses,  and  for  the  severity  of  the 
attacks  to  increase  rather  than  to  diminish ;  on  the  other 
hand,  cases  are  sometimes  met  with  in  which  there  is  no  re- 
currence.    Provided  then  that  the  cardiac  or  vascular  disease 


686  '  Diseases  of  the  Heart. 

is  not  serious  and  does  not  progress,  and  that  the  patient  is 
able  to  avoid  the  exciting  causes  of  the  attack,  he  may  live 
for  years,  and  enjoy  a  fairly  comfortable,  and  even  active  ex- 
istence. I  have  met  with  two  or  three  cases,  in  which  several 
attacks  of  typical  and  severe  angina  pectoris  (which  there  is 
every  reason  to  believe  were  associated  with  degenerative 
changes  in  the  aorta  and  probably  in  the  coronary  arteries), 
have  occurred,  and  in  which  the  patients  have  not  only  con- 
tinued to  live  for  some  years,  but  have  also  continued  to 
lead  active,  and  indeed  laborious  professional  lives.  Such 
cases  are,  however,  the  exceptions  not  the  rule.  In  all  cases 
of  typical  angina  pectoris  after  forty  years  of  age,  the  prog- 
nosis should  be  most  guarded,  more  especially  if  there  is  any 
evidence  of  degenerative  arterial  change. 

The  prognosis  of  the  functional  form  of  angina  pectoris  is 
favourable. 

Treatment. —  In  treating  any  paroxysmal  affection,  we 
must  endeavour : — Firstly,  to  relieve  the  paroxysm,  and 
secondly,  to  prevent  its  recurrence,  and  to  cure  the  condition 
on  which  it  depends. 

The  relief  of  the  paroxysm. — To  Dr  Lauder  Brunton  belongs 
the  great  merit  of  having  discovered  that  the  arterial  blood 
pressure  is  increased  in  many  cases  of  angina  pectoris,  and 
that  by  the  administration  of  nitrite  of  amyl  inhalations,  the 
paroxysm  may  often  be  steadily  and  completely  relieved. 
Subsequent  observations  have  abundantly  confirmed  Dr  Brun- 
ton's  discovery,  which  is  one  of  the  most  important  thera- 
peutic advances  of  our  time.  ]The  drug  acts  by  suddenly 
reducing  the  arterial  tension  or  spasm  on  which  the  paroxysm 
primarily  depends.  )  Since  angina^pectoris  may  be  produced 
by  several  different  conditions,  |_nitrite  of  amyl  is  not,  of 
course,  a  specific^  It  may  be  expected  to  be  effective  in 
those  cases  in  which  the  blood  pressure  is  high  during  the 
paroxysm,  and  in  which  the  main  object  of  treatment  is  to 
produce  a  rapid  reduction  of  the  increased  pressure.  Three 
drops  should  be  poured  upon  a  handkerchief  or  piece  of 
blotting  paper    and    inhaled    during   the    attack.     In   many 


Treatment  of  Angina  Pectoris.  687 

cases  a  larger  dose  (5-10  drops)  is  required,  but  the  smaller 
quantity  should  first  be  tried,  for  some  people  are  unusually 
susceptible  to  the  drug.  A  patient  who  has  once  had  an 
attack  of  angina  pectoris  should  always  carry  some  nitrite 
of  amyl  about  with  him  ;  the  remedy  may  be  had  in  glass 
capsules,  and  should  a  paroxysm  come  on,  it  is  only  ne- 
cessary to  break  one  of  the  capsules  in  the  handkerchief  and 
inhale  the  drug. 

Another  most  valuable  remedy,  which  also  acts  by  reduc- 
ing the  arterial  tension,  is  nitro-glycerine.  We  are  indebted  for 
most  of  our  knowledge  with  regard  to  the  value  of  this  drug 
in  angina  pectoris  to  Dr  Murrell.  One  drop  of  a  i  per  cent, 
spirituous  solution,  or  a  lozenge  containing  the  y^gt^"^  P^^'t 
of  a  grain  may  be  given  three  times  daily.  IThe  remedy  is 
particularly  useful  in  those  cases  in  whicii  the  arterial 
tension  is  habitually  high,  and  in  which  repeated  paroxysms 
of  angina  are  apt  to  occurTl  It  is  more  valuable,  therefore,  as 
a  preventative  of  the  paroxysms  than  for  the  relief  of  the 
paroxysm  itself ;  it  acts,  however,  in  both  ways.  It  is  inferior 
to  nitrite  of  amyl  for  the  rapid  reduction  of  arterial  blood 
pressure  ;  for  the  relief  of  the  paroxysm  itself,  therefore, 
nitrite  of  amyl  is  to  be  preferred. 

In  those  cases  in  which  nitrite  of  amyl  inhalations  fail  to 
relieve  the  attack,  and  in  cases  in  which  it  is  not  at  hand, 
recourse  must  be  had  to  other  measures.  jThe  administration 
of  a  full  dose  of  ether,  brandy,  ammonia,  or  other  diffusible 
stimulant  ;\  the  subcutaneous  injection  of  a  full  dose  of 
morphia; 'and  more  especially  the  inhalation  of  chloroform  or 
ether,  are  the  measures  which  are  most  efficacious.  .  The 
application  of  a  mustard  blister  to  the  praecordial  region  is 
often  useful.  Professor  Peter  speaks  highly  of  local  depletion 
by  means  of  leeches  applied  to  the  prsecordia. 

TJie  prevention  of  the  recnrrenee  of  the  attack. — In  order  to 
prevent  the  recurrence  of  the  paroxysm,  it  is  essential  to 
avoid  the  exciting  causes  of  the  attack,  to  raise  the  general 
health  to  the  highest  possible  state  of  efficiency,  and  to  treat 
any  organic  lesion  of  the  heart,  blood-vessels,  or  other  organs 
which  may  be  present. 


688  Diseases  of  tJie  Hca7't. 

When  the  arterial  tension  is  habitually  high,  nitro-glycerine 
should  be  given  for  several  days  in  the  manner  recommended 
above  ;  and  the  general  measures,  such  as  occasional  purga- 
tion, restriction  of  the  food  and  drink,  etc.,  which  are  useful 
in  the  treatment  of  chronic  conditions  of  high  arterial  ten- 
sion^ employed. 

VPatients  who  have  had  an  attack  of  angina  pectoris  should 
be  impressed  with  the  gravity  of  the  affection  (though  in 
.severe  cases  any  such  advice  is  quite  unnecessary,  for  the 
agony  of  the  attack  is  so  fearful  that  they  know  full  well  of 
themselves  that  a  recurrence  may  prove  fatal),  and  of  the 
necessity  of  avoiding  anytliing  which  is  likely  to  suddenly 
increase  the  blood  pressurejy  All  sudden  efforts  must  be  care- 
fully avoided.  Persons  of  an  excitable,  irritable,  and  hasty 
temper  are  very  difficult  to  treat,  and  it  is  all  the  more 
important  to  impress  them  with  the  absolute  necessity  of 
avoiding  all  causes  of  mental  excitement,  and  of  living,  so  far 
as  their  disposition  will  permit,  placid,  quiet,  and  cheerful 
lives.  I  The  diet  should  be  easily  digestible,  but  at  the  same 
time  nutritious,  the  quantity  of  food  taken  at  a  meal  should  be 
strictly  moderate,;  in  short,  great  care  must  be  taken  to  avoid 
distention  of  the  stomach,  flatulence,  dyspepsia,  etc]'  ^iNervine 
tonics  and  anti-neuralgic  remedies  are  in  many  cases  most 
useful.  Arsenic  is  a  valuable  remedy  both  in  the  organic 
and  functional  forms  of  the  disease.  Quinine  and  iodide  of 
potassium  may,  in  some  cases,  be  given  with  advantage.  ] 

Duchenne  claimed  to  have  cured  angina  pectoris^  the 
local  application  of  the  faradic  current ;  and  Eulenberg  speaks 
highly  of  the  advantages  of  galvanism.  '  If  correctly  em- 
ployed it  is  probably,'  he  states,  *  a  remedy  of  chief  import- 
ance, and  perhaps  the  only  direct  remedy  for  angina 
pectoris.  But  the  nature  of  the  symptoms  will  direct  us 
when  to  select  methods  of  application  which  produce  reflex 
excitation  of  the  regulator  nerves  of  the  heart,  and  when  to 
prefer  direct  galvanization  of  the  cervical  sympathetic  and 
cervical  vagus.  I  have  only  been  able  to  use  the  former  pro- 
cedure in  three  cases  of  accelerated  action  of  the  heart  without 
organic  disease, — but  could  not  continue  the  application  long 


Treatment  of  Angina  Pectoris.  689 

in  either  instance.  The  effect  was  distinctly  good  ;  the 
attacks  became  less  severe  ;  and  in  one  case,  ceased  entirely, 
while  previously  they  had  made  their  appearance  almost 
daily.  In  a  fourth  case,  recently  brought  under  treatment, 
the  attacks  have  become  rarer  and  milder.  The  method  used 
consists  in  the  application  of  strong  stabile  currents,  rising  to 
the  number  of  30  elements  ;  the  positive  pole,  with  a  broad 
surface,  is  placed  upon  the  sternum,  while  the  negative  is 
placed  on  the  lower  cervical  vertebrae.  Von  Heubner  has 
lately  obtained  a  permanent  cure  by  similar  methods  in  a 
case  which  seemed  to  have  a  rheumatic  origin.  He  placed 
the  positive  electrode  upon  the  fossa  supra  sternalis,  and  the 
negative  upon  the  cervical  ganglia  of  the  sympathetic,  on 
both  sides  in  succession  ;  then  he  placed  the  positive  pole 
upon  the  lowest  cervical  ganglion,  and  the  negative  upon  the 
sensitive  spots,  at  the  angles  of  both  shoulder-blades.  At 
first  only  very  weak  currents,  of  from  4  to  6  elements,  were 
borne.  The  attacks  ceased  from  the  first  session,  and  did  not 
return  ;  and  by  degrees  it  became  possible  to  use  stronger 
currents,  of  from  8  to   10  elements.'' 

Electric  treatment  is  most  likely  to  prove  useful  in  the 
functional,  and  more  purely  neurotic  forms  of  the  disease.  In 
the  organic  forms,  one  of  the  most  important  points  is  to  treat 
the  cardiac  or  arterial  lesion  which  happens  to  be  present. 
The  greatest  attention  must  always  be  given  to  this  point, 
but  it  is  unnecessary  to  enter  into  details  which  will  be  found 
under  the  heads  of  aortic  v^alvular  lesions,  aneurism,  atheroma, 
pericarditis,  fatty  heart,  etc. 

In  treating  the  functional  forms  of  angina  pectoris,  the 
condition  of  the  general  health  must  be  carefully  attended  to. 
Careful  inquiry  m.ust  be  made  into  the  habits  of  the  patient, 
excesses  of  all  kinds  forbidden,  anaemia  treated,  in  short,  the 
general  and  special  treatment  which  is  advisable  in  any  case 
of  ordinary  neuralgia  carried  out. 

■'  Ziciiisseii's  Cyclopiedia^  vol.  xiv.  p.  54. 


X    X 


690  Diseases  of  tJie  Heart. 


CHAPTER    VII  I. 

DISEASES  OF  THE  THORACIC  AORTA  ACUTE  AORTITIS.  ATHEROMA. 
GENERAL  DILATATION.  ANEURISM.  COARCTATION  OF  THE  AORTIC 
ARCH. 

Thk  more  important  affections   of  the  thoracic   aorta  which 
call  for  consideration  are  : — 

1.  Acute  inflammation,  or  acute  aortitis,  as  it  is  termed. 

2.  The  chronic  inflammatory  and  degenerative  processes 
and  their  results,  amongst  which  the  most  important  are 
atheroma,  general  dilatation,  and  aneurism. 

The  reader  is  particularly  recommended,  before  com- 
mencing the  study  of  the  individual  diseases  of  the  aorta,  to 
refer  to  the  description,  which  has  been  previously  given,  of 
the  anatomical  relations  of  the  aorta  and  of  the  clinical 
methods  by  which  its  condition  is  investigated  (see  page  224). 

ACUTE  AORTITIS. 

Acute  inflammation  of  the  outer  coat  of  the  aorta  is 
sometimes  observed  as  the  result  of  inflammation  of  the 
surrounding  parts — the  pericardium  and  mediastinal  tissues. 
Acute  inflammation  limited  to  the  aorta,  and  involving  the 
whole  thickness  of  its  wall,  is  of  very  rare  occurrence  ;  no 
case,  either  during  life  or  after  death,  has  come  under  my  own 
observation,  which  I  could  distinctly  recognise  as  answering 
to  the  descriptions  which  have  been  given  of  the  condition. 

Symptoms  and  physical  signs. — Fever,  with  rigors  and 
general  uneasiness,  throbbing  pulsation,  and  (in  some  cases) 
severe  pain  in  the  region  of  the  aorta,  tumultuous  action  of 
the  heart,  disturbances  of  breathing,  and  symptoms  due  to 
embolic  infarctions  in  distant  parts,  a  tendency  to  syncope, 
and  apprehension  of  impending  death,  are  some  of  the  more 


Diagnosis  and  Treatment  of  Acute  Aortitis.    691 

prominent    symptoms  which  have    been  noticed  in  cases  of 
supposed  acute  aortitis. 

Th.Q  physical  signs  are  indefinite,  and  are  often  complicated 
with  those  of  cardiac  disease  ;  throbbing  pulsation  of  the 
aorta,  irregular  and  tumultuous  action  of  the  heart,  a  systolic 
aortic  murmur,  and  the  secondary  physical  signs  due  to 
embolic  infarctions,  are  probably  the  most  important. 

Diagnosis. — Acute  aortitis  can  seldom,  if  ever,  be  posi- 
tively recognised  during  life.  According  to  Walshe,  'pain, 
thrill,  and  pulsation  in  the  course  of  the  vessel,  with  arterial 
murmur  coasting  the  spine,  and  answering  in  localisation 
neither  to  a  murmur  of  the  aortic  nor  of  the  mitral  valves, 
would  be  the  conditions,  coupled  with  great  distress  and 
pyrexia,  most  nearly  warranting  the  diagnosis  of  the  disease. 
But,'  he  adds, '  it  is  needless  to  point  out  the  varieties  of  states 
that  might  simulate  the  entire  series,  except  the  aortic 
murmur,  and  in  respect  to  this  murmur  the  possibility  of  its 
depending  upon  chronic  disease  proclaims  the  necessity  of 
caution.'^ 

Treatment. — The  application  of  leeches,  and  cold  in  the 
form  of  icebags,  over  the  course  of  the  aorta,  together  with  the 
internal  administration  of  antipyretic  remedies,  and  of  opium, 
aconite,  digitalis  and  belladonna,  in  accordance  with  the  special 
requirements  of  each  case,  seem  the  measures  most  worthy 
of  recommendation.  The  same  treatment,  which  has  been 
recommended  for  acute  endocarditis,  may  also  be  employed. 

ATHEROMA  AND   GENERAL   DILATATION    OF    THE   AORTA. 

Atheroma  of  the  aorta  is  of  very  common  occurrence, 
and  is,  in  many  cases,  associated  with  disease  of  the  aortic 
valve.s,  general  or  local  dilatation  (aneurism)  of  the  aorta,  and 
atheroma  of  the  coronary  arteries  and  peripheral  vessels. 

Aitiology  and  Pathology. — General  atheroma,  except  the 
form  which  results  from  syphilis,  is  essentially  a  senile  change, 

'  Diseases  of  the  Heart,  fourth  udition,  j).  472. 


692 


Diseases  of  the  Heart. 


and  is  seldom  seen  in  an  advanced  degree  before  the  age 
of  forty-five,  though  fatty  spots  at  the  base  of  the  aorta  are 
sometimes  met  with  in  quite  }'oung  subjects,  and  general 
dilatation  and  inflammation  of  the  aortic  arch  may  develop 
in  comparatively  young  persons,  as  the  result  of  strain  and 
aortic  incompetence. 

Males  are  much  more  frequently  affected  with  atheroma 
than  females. 

The  great  causes  of  the  condition  are  strain  (more 
especially  frequently  repeated  and  sudden  increases  of  the 
blood  pressure),  syphilis,  alcoholic  excesses,  gout,  rheuma- 
tism, exposure  to  cold,  and  depressing  influences  of  all  kinds. 
The  condition  seems  sometimes  to  be  hereditary. 


Fig.   zbd,.—  Section  through  a  gelatinous  spot  in  a  case  of  atheroma.     (  x    180. ) 

a,  free  surface  of  the  aorta  at  the  summit  of  the  gelatinous  patch  ;  b,  free  sur- 
face of  aorta  at  the  side  of  the  gelatinous  patch  ;  c,  elastic  lamina  ;  d,  round  cells ; 
e,  spindle  cells  ;  /,  collection  of  oil  globules  in  the  midst  of  fibrous  tissue. 


Pathology  of  Atheroma.  693 

PatJiology. — In  the  earlier  stages  of  the  process,  opaque, 
yellow  patches,  or  raised  gelatinous-looking  nodules  of  a 
pinkish-grey  colour,  are  seen  scattered  here  and  there,  on  the 
interior  of  the  aorta.  On  microscopicat  examination,  the 
gelatinous  patches  are  found  to  consist  of  spindle-shaped 
cells,  and  of  round  cellular  elements  which  stain  deeply  with 
picro-carmine,  and  which  are  for  the  most  part  arranged  in 
rows,  parallel  to  the  long  diameter  of  the  vessel.  (See  fig. 
264.) 

As  the  disease  advances,  collections  of  fatty  particles 
are  seen,  more  especially  in  the  deeper  layers  of  the  inner 
coat ;  ultimately  the  tissue  is  in  places  completely  destroyed, 
and  the  broken  down  fatty  debris  is  collected  in  cavities,  to 
which  the  term  atheromatous  foci  has  been  given  ;  calcareous 
particles  are  at  the  same  time  deposited  (see  fig.  265) ;  the 
middle  and  outer  coats  are  generally  infiltrated  here  and  there, 
with  round  cells,  and  the  nutrient  vessels  of  the  aorta  are 
often  found  to  be  undergoing  obliteration,  i.e.  to  be  affected 
with  endarteritis  obliterans. 

The  naked-eye  appearances  which  the  aorta  presents  are 
now  striking;  the  vessel  is  usually  more  or  less  dilated,  the 
dilatation  being  sometimes  general  and  uniform,  in  other 
cases  partial  and  local ;  its  interior  is  studded  here  and  there 
with  hard  projecting  nodules,  some  of  which  have  the  con- 
sistency of  cartilage,  others  being  hard  and  dense  like  bone, 
the  latter,  which  are  in  reality  calcareous  plates,  are,  for  the 
most  part,  thin  and  brittle;  fissures,  cracks,  and  small  irregular 
ulcers,  which  communicate  with  atheromatous  foci  in  the 
subjacent  tissue,  are  frequently  seen  in  the  interior  of  the 
aorta  ;  not  unfrequently  the  sharp  edge  of  a  thin  calcareous 
plate  projects  through  the  ruptured  lining  membrane,  and  the 
blood  is  seen  to  have  made  its  way  into  the  atheromatous 
cavities  and  between  the  coats  of  the  artery,  forming  a  small 
dissecting  aneurism. 

PatJwlogical  pliysiology.—  The  effect  of  the  atheromatous 
process  is  to  impair  the  elasticity  and  resisting  power  of 
the  aortic  wall ;  local  or  general  dilatation  of  the  vessel  is 
consequently  very  apt  to   occur  under  the  influence   of  the 


>  ' 


Fig.  265. — Section  through  tlic  ivholc  thickness  of  the  aorta  ?';/  atheroma. 
(  X  about  40. ) 
I,  inner  ;  2,  middle  ;  and  3,  outer  coats  ;  a,  free  surface  of  lining  membrane  ; 
b,  /',  fatty  particles  ;  c,  fat  crystals  ;  (/,  leucocytes  surrounding  vessel  of  middle 
coat ;  e,  leucocytes  in  outer  coat  ;  f,  outer  surface  of  vessel.  _ 


Syviptoins  and  Physical  Signs  of  Atheroma.  695 

blood-pressure.  But  the  effects  of  the  atheromatous  process 
are  seldom  limited  to  the  aorta  itself  ;  in  many  cases  the 
aortic  valves  are  involved,  and  the  peripheral  blood-vessels 
and  coronary  arteries  similarly  affected  ;  secondary  changes 
(hypertrophy,  dilatation,  and  in  some  cases  mitral  incom- 
petence) are  often,  therefore,  present  in  the  heart. ^ 

Syinptonis. — Symptoms  may  be  entirely  wanting,  and  this 
is  more  particularly  the  case  when  the  disease  is  confined  to 
the  aorta  itself,  i.e.  when  the  peripheral  vessels  are  not  affected, 
when  the  aortic  valve  is  not  incompetent,  and  when  the 
coronary  circulation  is  not  interfered  with. 

When  the  peripheral  blood-vessels  are  affected,  symptoms 
and  signs  of  defective  cerebral  circulation  (giddiness,  fainting 
fits,  irritability  of  temper,  defective  cerebration,  etc.)  are  of 
frequent  occurrence. 

When  the  aortic  arch  is  dilated,  shortness  of  breath  and 
other  symptoms  of  intra-thoracic  pressure  may  be  present. 

When  the  root  of  the  aorta  is  affected,  and  more  especially 
when  the  coronary  arteries  are  involved,  or  the  branches  of 
the  coronary  plexus  which  ramify  over  the  root  of  the  aorta 
implicated,  pain  of  an  angina-like  character  or  attacks  of  true 
angina  pectoris  may  occur. 

Embolic  symptoms  arc  in  some  cases  observed,  portions 
of  fibrine,  which  have  been  deposited  on  the  roughened  surface 
of  the  aorta,  being  detached  and  carried  to  some  distant 
vessel. 

When  the  aortic  valve  is  incompetent,  when  the  left 
ventricle  has  become  dilated,  or  the  mitral  valve  incompetent, 
other  symptoms  will  of  course  be  observed.- 

Physical  signs. — In  those  cases  in  which  the  aortic  arch  is 
of  normal  size,  and  in  which  there  are  as  yet  no  secondary 

'  The  secondary  cardiac  changes  met  with  in  atheroma  of  the  aortic  arch,  may 
be  due  to : — [a)  the  difficulty  which  the  blood  has  in  passing  through  the  rigid 
vessels ;  {l>)  aortic  incompetence,  which  is  often  present ;  (c)  obstruction  to  the 
coronary  circulation,  which  may  be  present  in  consequence  of  narrowing  of  the 
orifices  or  atheromatous  disease  of  the  trunks  of  the  coronary  arteries. 

^  See  the  articles  on  aortic  regurgitation,  dilatation  of  the  left  ventricle,  etc. 


696  Diseases  of  tJie  Heart. 

alterations  in  the  left  heart,  physical  signs  may  be  entirely 
wanting  ;  in  cases  of  this  description  the  aortic  second  sound 
is  very  often  acv^entuated,  in  consequence  of  the  obstruction 
to  the  blood-flow  through  the  aorta  and  peripheral  vessels. 

When  the  aortic  arch  is  dilated,  increased  dulness  over 
the  manubrium  sterni  and  pulsation  in  the  supra-sternal 
notch  can  usually  be  detected  ;  a  systolic  murmur  is  in  many 
cases  audible,  and  a  systolic  thrill  can  sometimes  be  felt,  over 
the  course  of  the  aorta  ;  in  these  cases,  the  aortic  second 
sound  is  often  loudly  accentuated. 

When  the  aortic  valve  is  incompetent,  and  when  secondary 
changes  (hypertrophy,  dilatation,  etc.)  have  taken  place  in  the 
heart,  other  physical  signs  will  of  course  be  present. 

In  those  cases  in  which  the  atheromatous  process  involves 
the  smaller  arteries,  the  radials,  temporals,  and  other  super- 
ficial vessels  may  stand  out  like  tortuous  cords  ;  the  thickening 
and  rigidity  of  their  coats  can  be  felt  when  they  are  compressed 
by  the  finger ;  the  tidal  wave  in  the  sphygmographic  tracing 
is  unusually  prominent.     (See  fig.  266.) 


l-'iG.  266. — Atheroma  and  Aneurism  of  Aortic  Arch. — J-  D-,  fet.  52,  admitted  to 
Newcastle  Infirmary  21st  February  1878,  suffering  from  aneurism  of  the 
ascending  portion  of  the  aortic  arch  and  atheroma.  The  tidal  wave  is  very 
strongly  marked.  There  was  no  perceptible  difference  between  the  two 
pulses. 

Diagnosis. — The  opinion  must  be  entirely  based  upon 
the  physical  condition  of  the  aorta  and  of  the  peripheral 
vessels.  The  facts,  that  the  patient  has  passed  the  prime  of 
life  ;  that  indications  of  tissue  degeneration,  such  as  the  arcus 
senilis,  are  present  ;  a  history  of  syphilis,  gout,  alcoholic 
excess,  and  exposure  to  want  and  pri\^ation,  afford  corrobo- 
rative evidence  in  doubtful  cases. 


Pi'ognosis  and  Trcatiucnt  of  Atheroma  of  tJie  Aorta.  697 

Pi'ognosis. — So  far  as  is  at  present  known,  atheroma  is  an 
incurable  condition  ;  the  opinion  as  to  the  probable  duration 
of  the  case  must  be  chiefly  based  upon:  (i)  the  extent  of  the 
disease,  as  evidenced  by  the  condition  of  the  aorta  and  super- 
ficial vessels  ;  (2)  the  circumstances,  habits,  and  surroundings 
of  the  patient — whether  he  is  able  to  lead  a  quiet  '  strainless  ' 
life,  his  alcoholic  tendencies,  etc.  ;  (3.)  the  condition  of  the 
aortic  valves  and  of  the  heart. 

The  opinion  must  always  be  guarded,  for  sudden  accidents 
which  it  may  be  impossible  to  foresee  (such  as  the  bursting  of 
a  cerebral  blood  vessel,  embolic  plugging  of  a  cerebral  vessel, 
the  rupture  of  an  aortic  aneurism  too  small  for  detection,  or 
the  occurrence  of  cardiac  syncope),  may  at  any  time  occur. 

Treatment.— The  main  objects  of  treatment  are  to  keep 
the  circulation  as  quiet  as  possible,  and  to  maintain  the  con- 
dition of  the  general  health.  Everything  likely  to  increase 
the  blood-pressure  within  the  aorta  must  be  carefully  guarded 
against,  but  the  rigid  system  of  rest,  which  will  afterwards 
be  recommended  for  the  treatment  of  aortic  aneurisms,  is 
neither  necessary  nor  desirable.  The  treatment  must,  of  course, 
be  conducted  in  accordance  with  the  condition  of  the  heart, 
and  the  special  requirements  of  each  individual  case  ;  when, 
for  instance,  symptoms  and  signs  of  cardiac  dilatation  and 
failure  arise,  digitalis  and  stimulants,  remedies  which  are  to  be 
avoided  in  the  earlier  stages  of  the  case,  must  be  prescribed. 
It  is  unnecessary  to  enter  into  details  which  the  reader  who 
is  familiar  with  the  treatment  of  cardiac  valvular  lesions 
and  of  aortic  aneurisms,  will  readily  supply  for  himself. 

ANEURISM  OF  THE  THORACIC  AORTA. 

Aneurism  of  the  thoracic  aorta  is  a  common  condition,  and 
is  of  great  practical  and  clinical  interest. 

Varieties. — Aneurisms  of  the  thoracic  aorta,  which  have 
not  perforated  the  chest,  are  almost  invariably  true  aneurisms, 
that  is  to  say,  the  aneurismal  sac  is  composed  of  one  or 
more  of  the  three  natural  coats  of  the  aorta  Tthe  interna,  the 


698  Diseases  of  tJie  Heart. 

media,  and  the  adventitia).  After  the  sac  perforates  the  chest 
wall,  blood  escapes  beneath  the  muscles  and  subcutaneous 
tissues,  and  a  false  aneurism  is  formed,  external  to  the  cavity 
of  the  thorax,  in  which  the  true  aneurism  is  situated.  Oc- 
casionally a  false  aneurism  is  formed  within  the  cavity  of  the 
chest  or  abdomen,  by  the  rupture  of  the  true  sac  and  the  escape 
of  blood  into  the  surrounding  parts.  It  is  rare  to  meet  with  a 
false  aneurism  of  this  description  within  the  chest,  and  it  is 
onl}^  likely  to  occur  in  the  presence  of  pleuritic  adhesions, 
which  place  a  limit  on  the  amount  of  blood  which  can  be 
extravasated.  Rupture  into  a  healthy  pleura  speedily  proves 
fatal.^  In  some  cases,  the  dilatation  of  the  aorta  is  general, 
and  the  aneurism  assumes  a  globular  or  fusiform  shape  ;  in 
others,  and  these  are  the  most  frequent,  the  bulging  is  partial, 
and  the  aneurism  is  said  to  be  saccular.  (See  fig.  267.)  ^ 
Occasionally  the  aneurism  bursts  into  a  vein,  to  these  cases 
the  term  artei'io-imious  aneurism  is  given.  When  the  internal 
coat  is  ruptured,  and  blood  escapes  between  it  and  the  media, 
or  between  the  different  layers  of  which  the  media  is  com- 
posed, the  aneurism  is  called  dissectiug.  A  combination  of 
these  different  forms  is  not  unfrequently  met  with  (see  figs. 
268  and  269),  in  which  there  are  three  aneurisms,  one  a  good 
example  of  the  globular  or  fusiform  variety,  and  the  other 
two  sacculated). 

Aitiology  and  Pathology. — The  great  causes  of  aneurism  of 
the  thoracic  aorta,  indeed  of  all  internal  aneurisms,  B-ve,  firstly, 
local  weakness  of  the  arterial  wall,  and  secondly,  increased 
arterial  blood  pressure. 

The  most  common  cause  of  local  weakness  of  the  aortic 
wall  is  chronic  endarteritis  (atheroma),  but  any  degeneration 
or  inflammation  either  of  the  internal,  the  middle,  or  the 
outer  coat,  will  produce  local  weakness,  and  will  therefore 
predispose  to  the  formation  of  aneurism.     Degeneration  of  the 

'  Occasionally  the  patient  survives  for  a  few  days. 

-  Aneurisms  of  the  abdominal  aorta  are  not  described  in  this  work,  but  this 
specimen  is  represented  because  it  is  more  typically  saccular  than  any  aneurism  of 
the  thoracic  aorta  which  I  possess. 


Fig.  267. 

Aneurism  of  the  Abdominal  Aorta,  involving  tlte  origins  of  the  cmliac  axis,  superior  mesenteric  and  renal 
arteries.  {Smaller  than  the  actual  specimen — a  dried  jrrejyaration.  Size  of  drawing,  5^  x  A\  in. ; 
size  of  specimen,  8^  x  7|  in."). 

a,  descending  thoracic  aorta ;  b,  abdominal  aorta  at  its  bifurcation ;  c,  inferior  mesenteric 
artery ;  d,  the  right,  and  e,  the  left  kidney ;  f ,  the  upper  sac  of  the  aneurism,  which  invol  voa 
the  origin  of  the  cseliac  axis ;  g,  the  lower  sac  from  which  the  main  branches  of  the  rena' 
arteries  spring ;  h,  h,  the  ureters. 


X 


r^«^ 


t. 


Pig.  268, 


Aneurism  involving  the  descending  Owradc  and  the  upper  part  of  the  Abdominal  Aorta.     (Front  vietc.) 
Smaller  than  the  dried  preparation.    Size  of  drawing,  6|  x  2i  in. ;  size  of  specimen,  13J  x  5^  in. 

a,  Termination  of  the  ascending  portion  of  the  aortic  arch ;  b,  a  portion  of  the  descending 
thoracic  aorta  situated  between  the  aneurismal  sacs  f  and  g ;  c,  abdominal  aorta  below  the 
aneurism ;  d,  the  diaphragm ;  e,  small  commencing  aneurism  at  the  junction  of  the  transverse 
•with  the  descending  portions  of  the  wch ;  f ,  globular  aneurismal  sac,  the  size  of  a  hen's  egg, 
involving  the  descending  thoracic  aorta;  g,  large  heart-shaped  aneurism,  springing  from  the 
descending  thoracic  and  the  abdominal  aortse, 

M=lj«««iCoiiMi»(i,U'«'  Em 


Fig.  269. 


Anewrism  involving  the  descending  thoracic  and  the  upper  part  of  the  Abdominal  Aorta.     (BckJ:  view.) 
Smaller  than  the  dn'ied  preparation.    Size  of  drawing,  6|  x  2  J  in. ;  size  of  specimen,  13^  x  ^^  in. 

a,  termination  of  the  ascending  portion  of  the  aortic  arch ;  b,  abdominal  aorta ;  c,  the 
diaphragm ;  d,  globular  aneurismal  sac,  involving  the  descending  thoracic  aorta ;  a,  large  heart- 
shaped  sac,  springing  from  the  descending  thoracic  and  the  abdominal  aortas  ;  f,  point  at  "which 
the  upper  sac  was  in  contact  with  the  spinal  column ;  g,  point  at  which  the  lower  sac  was  in 
contact  with  the  spinal  column.  A  septum  separates  the  two  sacs  internally.  The  spinal 
column  corresponding  to  the  points  f  and  g  was  eroded. 


Fig.  270. 


The  interior  of  the  Leji  VetUride  and  base  of  the  Aorta,  showing  an  Aneurism  arising  immediatelg 
above  the  aortic  valve.    (SUghtly  smaller  than  the  (Ktual preparation.') 

The  aneurism  ruptured  into  the  sac  of  the  pericardium  causing  instantaneous  death.  The 
letter,  a,  indicates  the  point  of  rupture.  The  aortic  valve  was  (relatively)  incompetent ;  tha  left 
ventricle  is  dilated  and  hypertrophied. 


M 

n 


I 


Fig.  272.- 


u 


y 


Fig.  271. 


Fig.  271. — Longitudinal  section  throvgh  the  wall  of  the  aorta  and  the  adjacent  wall  of  an  aneurism 
sprlwjlng  from  it.     (^About  10  diameters.') 

a,  inner  coat  of  aorta;  a',  a',  detached  portions  of  the  inner  coat;  J,  middle  coat  of  aorts 
at  h'  the  inner  coat  is  detached ;  c,  the  wall  of  the  aorta  at  the  orifice  of  the  sac  ;  d,  d,  greatly 
thickened  inner  coat,  lining  the  interior  of  the  aneurismal  sac ;  e,  e,  remains  of  the  middle  coat  in  the 
aneurismal  wall,  it  has  almost  entii-ely  disappeared :  y,  _/',  obliterated  blood  vessels  in  the  cellular 
tissue  (^)  which  lies  between  the  aorta  and  the  aneurism,  i.e.  in  the  outer  coat  of  the  aorta — for  the 
aneiirism  and  the  sac  wall  are  in  close  contact  here. 

Fig.  272. — Diagram  to  sliow  the  rthxHimship  of  the  aorta  and  the  aneurism.  The.  letter  o,  which  is 
placed  in  the  sac  of  the  aneurism,  points  to  the  part  of  the  sac  wall  represented  in  fig.  271 ;  6,  is 
placed  in  the  aorta. 


Fig.  274. 


Fig.  273. — Transverse  section  tkrimgh  onariery  affected  with  endarteritis  ob/ite runs— the  vessel  to  which 
the  leitcr  a  injig.  iibjjointf.   \MagniJied  about  180  diameters.) 

a  outer,  and  6,  middle  coats ;  c,  elastic  lamina ;  d,  d,  tissue  filling  up  the  vessel ;  e,  free  lumen 
which  still  remains  ;  /;  large  cells  lining  the  iuterior  of  the  diseased  vessel. 

Fig.  274. — Transverse  section  through  an  artery  in  endarteritis  obliterans — the  vessel  to  which  the  letter  f ' 
in  Jig.  271  points.     (^Magnified  about  230  diameter.^.) 

a,  a,'   unobliterated  spaces  in  the  centre  of  the  vessel ;  6,  6,  cellular  elements  filling  up  the 
lumen  of  the  vessel ;  c,  elastic  lamina. 

OStT  AD  »«"  tt  L|I«IJ0.  M",»H»1Cu«MI»0.1jIHC?EpC«! 


yEtiology  and  PatJiology  of  Thoracic  Aneurism.   699 

middle  or  muscular  coat  is  by  far  the  most  important  factor  ; 
and  as  far  as  my  observation  goes,  it  fully  confirms  that  of 
Cornil  and  Ranvier,  who  state,  that  in  all  spontaneous  aneu- 
rismal  sacs  the  middle  coat  has  either  partially  or  totally  dis- 
appeared. In  many  cases,  the  degeneration  of  the  media  is 
secondary  to  the  lesion  of  the  interna.  In  others,  the  disease 
of  the  middle  coat  is  primary,  and  is,  I  think,  in  some  cases 
due  to  an  obliterative  affection  (endarteritis  obliterans)  of  the 
nutrient  vessels  in  the  aortic  wall.  (See  fig.  273.)  If  this 
opinion  be  correct,  it  affords  an  explanation  of  the  manner  in 
which  syphilis  may  act,  in  the  production  of  aneurism.  Acute 
ulceration  of  the  inner  coat,  which  is  met  with  at  the  base  of 
the  aorta  in  some  cases  of  ulcerative  endocarditis,  is  another 
cause  of  aortic  aneurism  (see  fig.  168,  in  which  a  small  local 
dilatation  is  present  just  above  the  diseased  valves)  ;  but  in 
cases  of  this  description,  the  patient  seldom  survives  a  suffi- 
cient length  of  time  to  allow  the  aneurism  to  attain  any  but 
very  small  dimensions. 

It  follows  therefore  that,  anything  which  produces  arterial 
degeneration,  predisposes  to  the  formation  of  aneurism  : 
syphilis,  alcoholic  excesses,  increased  aortic  blood  pressure 
(whether  it  occurs  during  the  whole  period  of  the  cardiac 
cycle,  as  in  cirrhosis  of  the  kidney,  or  only  during  the  cardiac 
systole,  as  in  aortic  regurgitation),  strain,  a  laborious  occupa- 
tion, gout,  and  rheumatism,  are  the  chief  causes  of  the  con- 
dition. Increased  blood  pressure  tends  not  only  to  produce 
arterial  degeneration,  and  so  predisposes  to  the  production  of 
aneurism,  but  it  also  acts  directly  by  causing  the  degenerated 
and  weakened  part  to  give  way.  Sudden  increase  of  the  blood 
pressure  (such  as  is  produced  by  violent  muscular  exertion 
or  sudden  effort)  is  more  likely  to  produce  an  aneurism  than 
the  continued  high  blood  pressure,  for  example,  which  is 
seen  in  Bright's  disease.  And  this  is  more  especially  the 
case  when,  in  addition  to  the  violent  muscular  exertion,  which 
produces  a  sudden  increase  in  the  arterial  blood  pressure, 
the  arterial  circulation  is  impeded,  as,  for  instance,  it  is 
apt  to  be  in  soldiers  by  tight  and  badly  fitting  accoutre- 
ments.     In    rare   cases,  traumatic    injuries,  such  as  blows  on 


700  Diseases  of  tJic  Heart. 

the  chest,  falls,  etc.,  seem  to  be  the  direct  cause  of  the  con- 
dition. In  such  cases  the  artery  which  gives  way  was  probably 
already  diseased;  and  in  the  case  of  a  fall,  at  all  events,  it  is 
more  frequently  the  sudden  effort  which  the  patient  makes  to 
save  himself,  and  the  consequent  sudden  increase  in  the 
arterial  blood  pressure,  which  produces  the  aneurism,  rather 
than  any  direct  injury  to  the  arterial  coats. 

Thoracic  aneurisms  occur  more  frequently  between  the 
ages  of  thirty  and  forty-five  than  at  any  other  period  of  life, 
for  it  is  at  this  time  that  their  two  great  causes — arterial 
degeneration  and  strain — are  most  often  met  with  in  com- 
bination. The  condition  is  extremely  rare  before  the  age 
of  twenty,  and  is  seldom  seen  before  thirty  ;  for  although 
young  persons  are  frequently  exposed  to  strain,  their  arteries 
are  sound,  and  therefore  able  to  bear  a  sudden  increase  of  the 
blood  pressure.  After  the  age  of  fifty  the  condition  becomes 
less  common  ;  for  although  the  tendency  to  atheroma  in- 
creases with  the  age  of  the  patient,  the  circulation  in  old 
people  is  seldom  put  upon  the  stretch,  and  the  degenerated 
and  weakened  aorta  is  therefore  equal  to  the  strain  to  which  it 
is  exposed. 

Occupation  necessarily  exerts  a  very  important  influence 
upon  the  production  of  aneurism.  Soldiers  (who  frequently 
contract  s}'philis,  who  are  often  given  to  alcoholic  excesses, 
and  whose  arterial  pressure  is  apt  to  be  suddenly  raised  to 
a  \Q.xy  high  point  in  consequence  of  the  powerful  muscular 
exertions  and  sudden  efforts  which  they  have  to  make,  and 
the  tight-fitting  accoutrements  which  they  have  to  wear)  are 
more  liable  to  aneurism  than  any  other  class  of  the  commu- 
nity. Speaking  generally,  it  may  be  stated  that  all  laborious 
occupations  predispose  to  aneurism.  Prostitutes  suffer  from 
aneurism  much  more  frequently  than  other  females.  In  ex- 
ceptional instances,  of  which  I  have  previously  quoted  an 
example  (see  page  ^6),  the  tendency  to  thoracic  aneurism 
seems  to  be  hereditary. 

Any  part  of  the  thoracic  aorta,  from  its  commencement 
just  above  the  aortic  orifice  (sinuses  of  Valsalva,  see  fig.  270), 
to  its  termination  beneath  the  pillars  of  the  diaphragm,  may 


PatJiology  of  Thoracic  Aneurisms.  701 

be  affected ;  but  the  ascending  portion,  and  the  junction  of 
the  ascending  and  transverse  portions  of  the  aortic  arch,  are 
the  parts  of  the  vessel  which  are  most  frequently  involved.^ 
These  parts  of  the  aorta,  especially  the  ascending  portion  of 
the  aortic  arch,  receive,  as  it  were,  the  full  force  of  the  blood 
current,  as  it  is  discharged  from  the  left  ventricle,  and  are 
therefore  more  exposed  to  strain  than  other  parts. 

On  microscopical  examination,  the  wall  of  an  aneurism  is, 
in  most  cases,  found  to  be  composed  of  the  inner  and  outer 
coats  of  the  aorta,  modified  by  inflammation  or  degeneration, 
the  middle  having  totally  or  partially  disappeared.  At  the 
bottom  of  the  sac  the  middle  coat  is  not  seen,  but  at  the  neck 
of  the  sac  (see  fig.  271)  it  is  generally  present ;  it  tapers  away, 
and  finally  disappears  altogether,  as  the  aneurismal  wall  passes 
away  from  the  junction  of  the  sac  with  the  aorta.  The 
thickened  and  altered  inner  and  middle  coats  then  come  into 
direct  contact.  The  blood  vessels  in  the  outer  coat  are  often 
completely  or  partially  obliterated  by  endarteritis  deformans. 
Layers  of  fibrine,  in  which  white  blood  corpuscles  are  often 
embedded,  are  usually  found  lining  the  inner  surface  of  the 
sac,  and  seem  in  some  preparations  to  be  undergoing  a  process 
of  imperfect  organisation.  The  degenerated  and  thickened 
inner  coat  often  presents  fatty  and  atheromatous  changes,  or 
is  infiltrated  with  calcareous  deposits. 

Clinical  History. — In  considering  the  symptoms  and  physi- 
cal signs  of  aneurisms  of  the  thoracic  aorta,  it  is  important  to 
remember : — 

Firstly^  That  a  thoracic  aneurism  is  a  pulsating  tumour, 
which  is  placed  in  a  cavity,  the  walls  of  which  are,  for  the  most 
part,  rigid  ;  and  that,  as  the  tumour  increases,  it  necessarily 

'  The  term  true  used  formerly  to  be  applied  to  those  aneurisms,  the  walls  of 
which  are  composed  of  all  the  three  arterial  tunics  (interna,  media,  and  adven- 
titia) ;  we  now  know  that  the  media  is  almost  invariably  absent  at  the  seat  of 
greatest  dilatation,  i.e.  at  the  bottom  of  the  sac.  The  term  true,  as  applied  in  the 
text,  includes  all  those  aneurisms  in  which  any  of  the  proper  walls  of  the  artery 
still  remain  as  a  continuous  wall  over  the  sac,  in  opposition  to  the  term/alse,  in 
which  all  the  three  coats  have  ruptured,  and  the  contents  of  the  original  (true)  sac 
have  become  extravasated  into  the  surrounding  tissues. 


702  JJ/scascs  of  the  Heart. 

pushes  aside  and  presses  upon  the  surrounding  organs  and 
parts. 

Secondly,  That  the  results  of  this  pressure  are  partly  me- 
cJianical  (displacement  of  the  solid  organs  and  parts,  collapse 
or  constriction  of  hollow  organs,  such  as  the  lung  or  oesophagus) 
and  partly  vital  (irritation,  inflammation,  and  ultimately  de- 
struction and  absorption  of  tissue). 

Thirdly,  That  the  size  of  the  sac  is  constantly  undergoing 
changes  and  variations,  in  accordance  with  alterations  of  the 
blood  pressure  ;  and  that  the  direction,  in  which  the  aneurism 
extends,  is  apt  to  undergo  variations,  in  consequence  of  the 
fact,  that  first  one  part  of  the  sac  wall,  and  then  another, 
yields  before  the  internal  pressure.  In  consequence  of  these 
variations,  which  may  occur  with  considerable  rapidity,  a  struc- 
ture which  to-day  is  seriously  pressed  upon,  may  to-morrow 
be  much  less  seriously  implicated.  Rapid  modifications  in  the 
pressure  symptoms  are  not  unfrequently,  therefore,  observed. 
The  exact  nature  of  the  pressure-effects  varies  with  : — 

(i)  The  position  and  size  of  the  sac  ;  in  other  words,  with 
the  particular  organs  and  parts  which  are  exposed  to  the 
pressure. 

(2)  The  static  condition  of  the  sac,  the  degree  of  pressure 
which  is  being  exercised  {i.e.  the  internal  blood-pressure),  and 
the  particular  direction  in  which  the  sac  is  extending. 

Cases  of  thoracic  aneurism  may,  for  clinical  purposes,  be 
divided  into  three  great  groups. 

In  \hz  first  group  the  aneurism  is  entirely  latent.  In  cases 
of  this  description,  there  are  no  symptoms,  and  there  i}iay  be 
no  physical  signs.  (It  is  quite  possible,  however,  that  in  some 
cases  physical  evidence  of  aortic  or  cardiac  disease  would  be 
detected,  if  the  physician  had  occasion  to  make  a  careful  ex- 
amination of  the  chest.)  In  the  cases  included  in  this  group, 
the  aneurism  is  deeply  situated,  usually  of  small  size,  and  is 
not  exerting  injurious  pressure  on  any  of  the  surrounding 
parts. 

In  a  second  group  of  cases,  there  are  v^ery  distinct  symp- 
toms and  signs  of  intra-thoracic  pressure,  but  it  is  extremeh- 


Clinical  History  oj   TJiorack  Ancurisuis.      703 

difficult — it  may  be  impossible — to  determine  whether  the 
pressure  is  due  to  an  aneurismal  tumour  or  a  solid  intra- 
thoracic growth.  In  these  cases  the  aneurism  is  deeply 
situated,  and  the  physical  signs  are  obscure. 

In  a  third  group,  the  physical  signs  of  aneurism  are  very 
distinct,  and  there  usually  are  very  distinct  pressure  symptoms. 
In  such  cases  in  which  the  aneurism  is,  as  a  rule,  superficial, 
and  often  of  large  size,  the  diagnosis  is  easy  or  self-evident. 

Let  us  now  consider  the  exact  character  of  the  symptoms 
and  physical  signs,  which  may  be  present  in  cases  of  aneurism 
of  the  thoracic  aorta,  in  detail. 

Symptoms. — The  most  important  symptoms  of  aneurism  of 
the  thoracic  aorta  are  the  pressure  symptoms.  In  many  cases 
there  is  little  or  no  derangement  of  nutrition,  little  disturbance 
of  the  general  health.  It  is  impossible  to  insist  too  strongly 
upon  this  important  fact,  which  is  in  many  cases  of  great 
diagnostic  value.  Cases  are  again  and  again  met  with  in 
which  a  patient  who  is  muscular  and  well  nourished,  and  who 
presents  all  the  appearances  of  robust — it  may  be  of  plethoric — 
health,  is  found  on  examination  to  be  the  subject  of  aneurism. 
Thoracic  aneurism  is,  in  fact,  one  of  the  few  conditions  in 
which  a  disease,  which  may  at  any  moment  prove  fatal, 
may  fail  to  produce  any  external  manifestation,  even  to  the 
eye  of  the  most  accomplished  clinical  observer.  It  must 
not,  however,  be  supposed  that  in  all  cases  of  thoracic 
aneurism  the  condition  of  the  general  health  and  the  physi- 
ognomy of  the  patient  are  unaltered.  In  many  cases  the 
countenance  wears  a  worn  expression,  suggestive  of  internal 
suffering  or  of  repeated  attacks  of  pain.  In  some,  the  patient 
looks  exhausted,  and  is  more  or  less — but  seldom  profoundly 
— emaciated,  the  exhaustion  being  generally  due  to  long  con- 
tinued pain  or  sleeplessness  ;  while  the  emaciation  is  caused 
by  pressure  on  the  oesophagus  or  thoracic  duct,  or  by  some 
complication.  In  those  cases  in  which  the  sac  is  pressing 
upon  the  superior  cava,  the  face  may  be  swollen  and  the  lips 
livid.  Sometimes  the  physiognomy  is  suggestive  of  a  cardiac 
complication. 


704  Diseases  of  tJie  Heart. 

The  more  \xVi.^ox\.KX\\.  pressure  symptoms  are  as  follows  : — 
Pain. — Of  all  the  symptoms  of  aneurism  of  the  thoracic 
aorta  this  is  the  most  frequent.  In  many  cases  the  pain  is 
distinctly  intra-thoracic,  and  is  then,  I  believe,  generally  due 
to  irritation  of  the  fine  sensory  nerve  filaments  of  the  aorta 
itself,  or  of  the  surrounding  organs  on  which  the  sac  is  press- 
ing. In  these  cases  the  pain  is  usually  more  or  less  inter- 
mittent, but  it  is  not  sharp,  shooting  and  lancinating  in 
character,  and  is  not  so  distinctly  paroxysmal  as  the  pain  due 
to  pressure  on  a  large  nerve  trunk.  In  other  cases  the  pain 
is  more  constant,  and  is  referred  to  some  part  of  the  chest 
wall,  being  in  many  cases  very  localised,  and  presenting  a 
dull  boring  character.  Pain  of  this  description  is  generally 
due  to  pressure  on  the  chest  wall,  and  is  typified  by  pain  in 
the  back,  which  results  from  the  pressure  of  an  aneurismal 
sac  upon  the  spinal  column,  and  from  erosion  of  the 
vertebrae.  In  a  few  cases  in  which  the  pain  is  distinctly 
angina-like  in  character,  the  aneurism  usually  involves  the 
root  of  the  aorta,  and  the  pain  is  probably  due  to  the  pressure 
on  the  cardiac  plexus.  In  others  again,  the  pain  radiates 
\cry  distinctly  in  the  area  of  distribution  of  some  large 
nerve  trunk,  shooting,  for  example,  round  the  chest  along 
the  course  of  an  intercostal  nerve,  or  down  the  arm  in  the 
area  of  distribution  of  the  nerves  of  the  brachial  plexus. 
In  cases  of  this  nature,  the  pain  is  markedly  paroxysmal  and 
lancinating  in  character.  It  may  be  attended  wuth  some 
ansesthesia  of  the  skin  and  loss  of  motor  power  ;  it  presents, 
in  short,  the  ordinary  characters  of  pain,  which  is  due  to 
direct  irritation  of  a  common  sensory  motor  nerve  trunk. 

Dyspiicca,  coitg/i,  and  alterations  in  the  voice,  are  frequently 
observed  in  cases  of  thoracic  aneurism,  and  may  be  due  to  a 
variety  of  causes.  A  large  intra-thoracic  aneurism  necessarily 
interferes  with  the  expansion  of  the  lungs  and  the  free  play 
of  the  heart,  and  by  its  mere  size  acts  as  a  mechanical  cause 
of  shortness  of  breath  ;  but  dyspnoea — more  especially  the 
severe  forms  of  dyspnoea — cough,  and  other  respiratory  symp- 
toms, are  generally  due  to  local  irritation  caused  by  the  pres- 
sure of  the  sac  on  some  part  of  the  respirator}-  apparatus. 


Syniphvus  of  Thoracic  Aneurisiu. 


/^D 


Respiratory  symptoms  (dyspnoea,  cough,  etc.)  may  also,  of 
course,  be  due  to  associated  disease  of  the  lungs  and  heart. 

The  pressure  of  the  aneurismal  sac  on  the  lung  tissue  very 
frequently  produces  local  pleurisy,  in  consequence  of  which, 
adhesions  are  formed  which  bind  the  lung  to  the  thoracic 
wall.  When  the  lung  tissue  itself  is  pressed  upon  and 
irritated,  cough,  expectoration  (mucous,  muco-purulent  or 
bloody  in  character),  and  shortness  of  breath  (seldom  amount- 
ing to  dyspnoea)  are  usually  present.  If  the  symptoms  and 
signs  of  aneurism  are  absent  or  indistinct,  the  observer  may 
perhaps  suppose  that  he  is  dealing  with  a  case  of  phthisis. 
An  aneurism  which  is  pressing  upon  the  lung  may  ultimately 
burst  into  the  lung  tissue  ;  the  fatal  rupture  is  in  some  cases 
preceded  by  blood-tinged  or  rusty  expectoration,  a  symptom 
which  should  always  excite  grave  apprehension  when  it  occurs 
in  the  course  of  this  affection  [i.e.  of  aneurism). 

Pressure  on  a  main  bronchus  usually  produces  considerable 
dyspnoea,  which  in  some  cases  is  paroxysmal  ;  an  extremely 
irritable  and  troublesome  cough,  which  is  generally  attended 
with  a  copious,  thin,  watery  expectoration,  is  often  present. 
A  wheezing  sound  can  sometimes  be  heard  when  the  stetho- 
scope is  placed  over  the  position  of  the  compressed  bronchus. 
Pressure  on  a  main  bronchus  prevents  the  free  entrance  of 
the  air  into  the  lung,  the  respiratory  sounds  are  consequently 
indistinct  on  the  affected  side,  but  this  point  will  afterwards 
be  considered  more  in  detail. 

Pressure  on  the  trachea  usually  gives  rise  to  great  distress 
and  difficulty  in  breathing,  and  may  produce  the  most 
aggravated  form  of  orthopnoea.  Dr  Bristowe  is  of  opinion 
that  pressure  on  the  trachea  is  the  cause  of  the  sudden 
attacks  of  paroxysmal  dyspnoea,  which  occur  in  the  course  of 
some  cases  of  thoracic  aneurism,  and  which  not  unfreqently 
prove  fatal.  Aneurisms  of  the  transverse  portion  of  the 
aortic  arch  are  most  likely  to  produce  this  form  of  dyspnoea 
(which  is  by  many  observers  thought  to  be  the  result  of 
pressure  on  the  recurrent  laryngeal  nerve),  and  therefore  to 
cause  laryngeal  paralysis  or  spasm.  The  suddenness  of  the 
attack,  if  we  adopt   Dr  Bristowe's  view,  may  be  explained  by 

Y  Y 


7o6  Diseases  of  the  Heart. 

supposing  cither  that  there  is  a  rapitl  increase  in  the  pressure, 
with  consequent  rapid  tracheal  obstruction,  or  that  the  narrow 
sHt-hke  aperture  in  the  trachea,  which  is  the  result  of  the 
compression,  becomes  suddenly  obstructed  by  an  accumula- 
tion of  mucus.  Dyspnoea,  the  result  of  tracheal  compression, 
is  usually  accompanied  by  a  well-marked  stridor.  The  ob- 
server at  once  sees,  on  looking  at  the  patient,  that  there  is 
difficulty  in  getting  a  sufficient  quantity  of  air  into  the  chest. 
There  is  often,  in  addition  to  the  dyspnoea  and  stridor,  a 
troublesome  and  violent  cough.  It  is  sometimes  possible, 
by  altering  the  position  of  the  patient,  to  remove,  in  part  at 
least,  the  pressure  from  the  trachea,  and  so  to  relieve  the 
dyspnoea. 

Pressure  on  the  recurrent  laryngeal  nerve  is  another  very 
important  cause  of  difficulty  in  breathing  and  cough.  The 
dyspnoea  is  apt  to  occur  in  paroxysms,  and  in  some  cases 
seems  to  be  due  to  paralysis,  in  other  cases  to  spasm  of  the 
glottis.  Pressure  on  a  nerve  trunk  gives  rise  either  to  irrita- 
tion or  destruction  ;  irritation  of  a  motor  nerve  produces 
spasm,  while  destruction  causes  paralysis.  Now  the  left  re- 
current laryngeal  nerve  is  the  motor  nerve  which  supplies 
almost  all  the  muscles  of  the  left  side  of  the  larynx  ;  conse- 
quently when  it  is  irritated  by  the  pressure  of  an  aneurism  or 
any  other  cause,  spasmodic  contraction  of  the  left  vocal  cord 
is  produced.  When,  again,  the  pressure  is  more  considerable, 
and  the  nerve  fibres  are  destroyed,  paralysis  of  the  left  vocal 
cord  will  result.  These  changes  can,  of  course,  be  recognised 
with  the  laryngoscope.  In  quite  exceptional  cases  pressure 
on  the  left  recurrent  has  been  attended  with  bilateral  laryngeal 
paralysis.  A  hard,  dry,  barking,  clanging  cough,  which  is  in 
some  cases  paroxysmal,  is  also  produced  by  pressure  on  the 
recurrent  laryngeal  nerve.  The  voice,  too,  is  usually  hoarse, 
husky,  or  whispering ;  in  some  cases  complete  aphonia  is 
observed. 

Paroxysmal  attacks  of  dyspnoea,  resembling  asthma,  seem 
in  some  cases  to  be  due  to  irritation  of  the  pulmonary 
branches  of  the  vagus. 

Dysphagia    is    present    in     many    cases    of    intra-thoracic 


Syiuptoms  of  TJwracic  Aneitrisin.  707 

aneurism,  and  is  generally  due  to  compression  and  flattening 
of  the  oesophagus,  but  in  some  cases  it  seems  to  be  caused  by 
spasms  of  the  muscular  fibres  of  the  oesophagus.  The  diffi- 
culty in  swallowing  is  rarely  constant,  but  is  apt  to  vary  from 
time  to  time.  It  is  rarely  so  complete  as  the  dysphagia  which 
results  from  an  organic  stricture.  It  is  important  to  empha- 
sise the  fact,  that  a  bougie  should  never  be  passed  in  cases  of 
this  description,  lest  the  pressure  of  the  instrument  should 
rupture  the  aneurismal  sac  and  produce  fatal  haemorrhage. 
In  all  cases  of  dysphagia,  therefore,  before  passing  an  oesopha- 
geal bougie,  the  physician  should  make  a  careful  examina- 
tion of  the  chest,  and  should  satisfy  himself  that  the  difficulty 
in  swallowing  does  not  depend  upon  the  presence  of  an 
aneurism. 

Engorgement  of  the  superior  cava  and  its  branches,  and 
oedema  of  the  subcutaneous  cellular  tissue  of  the  head,  neck, 
upper  extremities  and  upper  part  of  the  thoracic  wall,  are  seen 
in  some  cases  of  thoracic  aneurism,  and  are  due  to  the  pres- 
sure of  the  sac  upon  the  superior  cava.  The  hard,  brawny 
swelling  of  the  subcutaneous  tissues  at  the  root  of  the  neck, 
to  which  the  term  '  collar  of  flesh'  has  been  applied,  is  some- 
times observed. 

Emaciation  may  result  from  pressure  on  the  thoracic 
duct ;  it  is,  however,  more  frequently  due  to  derangement 
of  the  functions  of  the  stomach  or  to  obstruction  of  the 
oesophagus. 

HiccongJi  and  paralysis  of  one-half  of  the  diaphragm  may 
be  caused  by  pressure  on  the  phrenic  nerve. 

Dyspepsia  is  sometimes  caused  by  pressure  on  the  vagus. 

Physical  signs. — The  physical  signs,  which  are  present  in 
cases  of  thoracic  aneurism,  vary  considerably  in  different 
cases.     They  may  be  divided  into  two  groups,  viz. : — 

1st.  The  primary  or  direct  physical  signs,  i.e.  the  physical 
signs  which  are  directly  derived  from  the  aneurism  itself. 

2d.  The  secondary  or  indirect  pJiysical  signs,  /.r.  the  physical 
signs  derived  from  the  altered  condition  of  the  organs  or 
parts    on   which    the    aneurismal    sac   presses,   and   from   the 


"oS  Diseases  of  tJie  Heart. 

secondary  alterations  in  the  circulation  behind  and  in  front  of 
the  aneurismal  dilatation. 

Primary  physical  signs. 

The  primary  physical  signs  depend  more  particularly 
upon  : — 

u)  The  size  of  the  sac. 

(2)  The  position  of  the  sac,  more  especially  its  relationship 
to  the  chest  wall. 

It  is  of  the  greatest  importance  to  remember  that  the  condi- 
tion of  the  lungs  exerts  a  most  important  influence  upon  the 
nature  of  the  physical  signs  ;  when,  for  example,  the  lungs 
are  emphysematous,  it  may  be  difficult  or  impossible  to  detect 
an  aneurism,  even  of  large  size,  by  physical  examination  : 
when,  on  the  contrary,  the  anterior  margins  of  the  lungs  arc 
retracted  and  the  aneurismal  sac  comes  in  contact  with  the 
chest  wall,  the  physical  signs  are  unusually  distinct. 

Inspection. — {a)  When  the  aneurism  is  of  small  size,  when 
it  is  deeply  situated  and  separated  from  the  chest  wall  by  the 
lung  tissue,  inspection  of  the  chest  yields  no  information. 

{U)  When  the  sac  is  in  contact  with  the  chest  wall,  but 
when  the  chest  wall  is  still  intact,  slight  prominence  and  pulsa- 
tion can  usually  be  seen  on  careful  examination.^ 

[c)  When  the  aneurism  has  eroded  the  chest  wall,  an 
external  pulsating  tumour  is  apparent.  The  size  of  the 
tumour  varies,  of  course,  in  different  cases  ;  it  not  unfre- 
quently  is  as  large  as  the  closed  fist,  and  in  some  cases  has 
been  known  to  attain  the  size  of  a  child's  head. 

The  position  of  the  pulsating  prominence  depends  upon 
the  part  of  the  artery  which  is  affected,  anci  the  exact  spot  at 
which  the  sac  'points.'  Aneurisms  of  the  ascending  aorta, 
for  example,  usually  perforate  the  chest  in  the  neighbourhood 
of  the  second  or  third  right  interspace  ;  aneurisms  of  the 
descending  portion  of  the  aortic  arch,  or  of  the  descending 

'  The  exact  manner  in  which  the  chest  is  to  be  inspected  in  order  to  detect 
slight  degrees  of  pulsation  and  prominence,  has  been  previously  described.  (See 
p.   228.) 


Physical  Signs  of  TJioracic  Aneurism.         709 

thoracic  aorta,  generally  '  point '  on  the  posterior  or  lateral 
wall  of  the  left  chest,  but  this  will  afterwards  be  considered 
more  in  detail.  The  base  of  the  prominence  is  usually  much 
broader  than  the  apex.  The  skin  over  the  surface  of  the 
prominence  may  be  quite  natural,  in  other  cases  it  is  tense, 
shining,  red  or  bluish  in  colour. 

Palpation. — {a)  When  the  aneurism  is  of  small  size,  or 
when  it  is  deeply  situated  and  separated  from  the  chest  wall 
by  lung  tissue,  palpation  of  the  chest  wall  over  the  sac  ma)- 
yield  no  information.  In  some  cases  deep  pulsation  can  be 
felt  by  the  bimanual  method  of  palpation  previously  described 
(see  p.  229) ;  in  others,  more  particularly  when  the  transverse 
portion  of  the  aortic  arch  is  affected,  pulsation  can  be  felt  in 
the  supra-sternal  notch. 

{b)  When  the  aneurismal  sac  is  in  direct  contact  with  the 
chest  wall,  but  when  the  chest  wall  is  not  perforated,  a  systolic 
impulse,  and,  in  some  cases,  a  diastolic  shock  can  be  felt  when 
the  hand  is  placed  lightly  over  the  position  of  the  sac.  A 
systolic  thrill  can  also  sometimes  be  perceived.  (This  sign  is 
more  frequently  present  in  cases  of  general  dilatation  than  in 
cases  of  saccular  aneurism.) 

(r)  When  the  sac  has  perforated  the  chest  wall,  the  pul- 
sating prominence  is  in  some  cases  soft,  fluid,  and  fluctuating  ; 
in  others  {i.e.  in  those  cases  in  which  the  external  sac  contains 
much  laminated  clot),  it  may  feel  firm  and  solid.  A  thin, 
external  sac,  must  of  course  be  handled  with  great  care.  The 
skin  covering  the  sac,  and  the  structures  forming  the  base  of 
the  external  sac  are  often  extremely  tender  to  the  touch. 

Percussion. — {a)  When  the  aneurism  is  of  small  size  or 
deeply  situated  and  separated  from  the  chest  wall  b)'  lung 
tissue,  more  especially  when  the  lungs  are  emphysematous, 
percussion  may  yield  negative  results. 

{U)  When  the  sac  is  in  contact  with  the  chest  wall  there  is 
dulness  on  percussion  and  a  feeling  of  increased  resistance 
over  the  sac.  The  position  of  the  dulness  depends  upon 
the  portion  of  the  artery  which  happens  to  be  affected,  and 


7IO  Diseases  of  the  Heart. 

the  part  of  the  chest  wall  with  which  the  sac  is  in  contact. 
The  dulncss  is  not,  of  course,  an  exact  indication  of  the  size 
of  the  sac,  for  some  part  of  the  tumour  is  always  separated 
from  the  chest  wall  by  resonant  lung  tissue.  When  the  chest 
wall  is  tender  to  the  touch,  or  when  there  is  a  thin-walled 
external  sac,  the  percussion  must  be  lightly  performed.  Im- 
paired resonance  may  be  detected  in  many  cases  in  which  the 
sac  is  not  in  direct  contact  with  the  chest  wall. 

Auscultation. — In  order  to  comprehend  the  exact  signifi- 
cance of  the  sounds,  which  may  be  heard  over  an  aneurismal 
sac,  it  is  essential  to  remember : — 

(i)  That  the  sounds  and  murmurs  which  are  generated 
within  the  heart,  more  especially  the  aortic  second  sound  and 
aortic  valvular  murmurs,  are  propagated  into  the  aorta,  and 
may  therefore  be  heard  over  the  position  of  the  aneurism. 

(2)  That  in  dilated  or  aneurismal  conditions  of  the  aorta, 
the  aortic  second  sound  is  very  frequently  accentuated  ;  and 
that  this  accentuated  second  sound  (which  is  produced,  be  it 
remembered,  at  the  aortic  orifice  and  not  in  the  sac  itself) 
may  be  heard  over  the  aneurismal  tumour. 

(3)  That  in  the  majority  of  cases  of  thoracic  aneurisms, 
no  new  sounds  are  generated  within  the  sac  itself 

(4)  That  in  the  minority  of  cases,  a  murmur  is  generated 
within  the  dilated  and  atheromatous  or  aneurismal  aorta  ;  and 
that  this  murmur  is  almost  invariably  systolic.  In  very  rare 
and  exceptional  cases,  a  diastolic  murmur  (generated  within 
the  sac  itself)  has  been  heard. 

Now  when  the  aneurismal  sac  is  small  or  deeply  situated, 
auscultation  may  afford  no  direct  evidence  of  its  presence. 
A  murmur  or  an  accentuated  second  sound  may,  it  is  true, 
be  heard  when  the  stethoscope  is  placed  over  the  surface  of 
the  chest  overlying  the  sac,  but  the  murmur  or  accentuated 
second  sound  is  not  louder  (nearer  to  the  ear)  than  it  would 
be  if  the  aneurism  were  not  present.  Accentuation  of  the 
aortic  second  sound  is  suggestive  of  the  presence  of  an 
aneurism,  but  in  the  absence  of  other  symptoms  and  signs  it 
is  of  no  great  value,  for   it   may  depend    upon  a  variety  of 


PJiysical  Signs  of  TJioracic  Aneurism.         711 

other  conditions.  In  other  words,  an  accentuated  second 
sound  is  not  direct  evidence  of  the  presence  of  an  aneurismal 
tumour.  An  accentuated  second  sound,  when  heard  over  a 
circumscribed  dull  area  in  the  course  of  the  aorta,  is  however, 
very  suggestive  of  the  presence  of  an  aneurism. 

When  an  aneurismal  sac  approaches  the  surface  of  the 
chest,  the  sounds,  which  are  generated  at  the  aortic  valve  or 
in  the  aneurismal  sac  itself,  are  of  course  brought  nearer  to 
the  ear.  When,  therefore,  sounds  or  murmurs  are  heard  over 
a  part  of  the  chest  wall,  at  which,  in  health,  the  aortic  cardiac 
sounds  are  feebly  or  indistinctly  heard,  the  presence  of  an 
aneurism  is  strongly  suggested,  but  by  no  means  proved  ;  for 
anything  which  facilitates  the  conduction  of  a  sound  between 
the  aorta  on  the  one  hand  and  the  chest  wall  on  the  other 
(such,  for  example,  as  a  solid  intra-thoracic  growth),  may  pro- 
duce the  like  result.  The  exact  value,  which  is  to  be  attached 
to  evidence  of  this  description,  depends  upon  : — 

(i)  The  cJiaracter  of  the  sounds. — An  accentuated  second 
sound,  a  double  murmur  or  a  diastolic  murmur,  would,  under 
such  circumstances  {i.e.  when  heard  over  a  part  of  the  chest 
at  which  under  normal  circumstances  the  aortic  or  cardiac 
sounds  are  indistinct)  be  strongly  suggestive  of  an  aneurism. 
A  systolic  murmur,  accompanied  by  a  well-marked  or  accen- 
tuated second  sound  would  also  be  in  favour  of  an  aneurism. 
But  a  systolic  murmur  alone,  i.e.  unaccompanied  by  a  well- 
marked  or  accentuated  second  sound,  is  of  little  or  no  value  ; 
in  fact,  other  things  being  equal,  it  would  be  more  likely  to  be 
produced  by  a  solid  intra-thoracic  tumour  compressing  the 
aorta,  than  by  a  dilated  or  aneurismal  condition  of  the  vessel. 
A  systolic  murmur  heard  in  the  back,  over  the  position  of  the 
descending  thoracic  aorta  is,  however,  of  great  importance 
from  a  diagnostic  point  of  view. 

(2)  TJie  position  at  tvhich  the  sounds  are  Jieard. — When  the 
sounds  or  murmurs  are  heard  over  the  course  of  the  aorta,  an 
aneurism  is  suggested  ;  when  they  are  heard  away  from  the 
course  of  the  aorta,  some  other  cause  of  increased  conduction 
is  probable. 

(3)  The  associated  symptoms  and  physical  signs. — In   many 


7 1  2  Diseases  of  the  Heart. 

doubtful  cases  the  significance  of  the  sounds  depends  entirely 
upon  the  associated  conditions.  In  those  cases,  for  example, 
in  which  a  solid  tumour  is  in  contact  with  the  aorta,  and  in 
which  the  aortic  sounds  are  conducted  with  increased  facility 
to  the  chest  wall,  the  conduction  of  the  lung  sounds  is  also 
facilitated  ;  bronchial  breathing,  in  such  instances,  may  often 
be  heard  over  the  position  of  the  tumour. 

This  point  will  be  further  considered  in  treating  of  the 
diagnosis. 

When  the  aneurismal  sac  is  in  direct  contact  with  the 
chest  wall,  or  when  it  has  perforated  and  produced  an  ex- 
ternal tumour,  the  shock  of  the  aneurismal  impulse  can  often 
be  distinctl}'  felt  when  the  ear  is  placed  on  the  stethoscope. 
A  jog  or  shock  of  this  description,  which  I  am  in  the  habit  of 
terming  a  shock-sound,^  is  \&xy  characteristic  of  a  large  thin- 
walled  superficial  sac.  In  most  cases,  the  shock  is  systolic  ;  in 
some  a  diastolic  shock,  which  is  even  more  characteristic  and 
distinctive,  may  also  be  perceived.  When  the  aortic  second 
sound  is  accentuated  or  when  a  murmur  is  produced  either 
at  the  aortic  orifice  or  in  the  sac  itself,  these  modifications 
may  of  course  be  heard  when  the  stethoscope  is  placed 
over  a  superficial  sac  which  is  in  contact  with,  or  has  per- 
forated the  chest  wall. 

Secondary  physical  signs. 

The  secondary  physical  signs  are,  as  I  have  previously 
pointed  out,  of  two  kinds,  viz. : — 

(i)  Those  which  are  produced  by  secondary  changes  in  the 
heart  and  circulation,  behind  and  in  front  of  the  aneurismal 
tumour  respective!}'. 

(2)  Those  which  are  derived  from  the  altered  condition  of 
the  organs  and  parts  (other  than  the  heart,  arteries,  and  veins) 
on  which  the  aneurismal  sac  presses. 

'  The  term  shock-sound  is  not  perhaps  very  elegant,  but  it  is  expressive,  and 
conveys  to  my  mind,  at  least,  the  fact  that  the  impression  which  is  perceived  by 
the  ear,  is  chiefly  that  of  shock,  accompanied  by  a  faint  and  almost  toneless 
sound. 


Physical  Signs  of  Thoracic  Aneurism. 


I  i  j» 


PJiysical  signs  due  to  alterations  in  the  heart  and  eirenlation. 

A.  Backivard  efj'eets. — An  aneurism  of  the  thoracic  aorta 
does  not  necessarily  produce  any  secondary  alteration  in  the 
condition  of  the  heart.  In  many  cases,  however,  cardiac  alte- 
rations are  present.  These  alterations  may  be  the  direct  result 
of  the  aneurism,  but  in  many  cases  they  are  merely  associated 
conditions,  the  aneurism  of  the  aorta  and  the  cardiac  lesion 
being  the  results  of  a  common  cause,  as,  for  instance,  atheroma. 

Hypertrophy  of  the  heart. — In  some  cases  the  heart  is  hyper- 
trophied  ;  the  enlargement  may  be  due  to  the  increased  diffi- 
culty which  the  left  ventricle  meets  with,  in  forcing  the  blood 
through  the  aneurismal  dilatation,  but  is  generally  the  result 
of  some  other  condition,  such  as  associated  valvular  disease, 
general  atheroma,  etc.  An  aneurism  of  the  thoracic  aorta  does 
not  necessarily,  therefore,  produce  hypertrophy  of  the  left  ven- 
tricle, and  this  is  more  particularly  the  case  when  the  aneurism 
is  saccular.  (In  cases  of  general  dilatation  of  the  aorta,  the  left 
ventricle  is  usually  hypertrophied.) 

Displacement  of  the  heart  is  very  frequently  observed.  The 
displacement  is,  as  a  rule,  downwards,  or  downwards  and  to 
the  left.  In  exceptional  cases  (as,  for  instance,  in  that  repre- 
sented in  figure  268)  the  heart  is  displaced  forwards. 

Incompetence  of  the  aortic  valve  is  very  often  met  with.  I  n 
some  cases,  the  incompetence  is  the  direct  result  of  the  aneu- 
rism, as,  for  instance,  in  those  cases  in  which  the  base  of  the 
aorta  is  affected  and  relative  incompetence  of  the  aortic  valve 
produced,  the  aortic  segments  themselves  being  healthy  (see 
fig  270).  In  most  cases  the  incompetence  is  only  an  asso- 
ciated condition,  and  is  not  the  direct  result  of  the  aneurism, 
the  two  conditions  (the  aneurism  and  the  aortic  incompetence) 
being  due  to  a  common  cause,  e.g.  atheroma  or  .syphilitic 
disease  of  the  aorta.  In  a  few  cases,  the  aortic  incompetence 
seems  to  be  the  cause  of  the  aneurism  ;  but  this  point  has 
been  previously  mentioned  under  the  head  of  aetiology. 

Pericarditis,  adhei'ent  pericardium. — Aneurisms  of  the 
thoracic  aorta,  more  especially  of  the  intra-pericardial  portion 
of  the  ascending  arch,  very  frequently  produce  pericarditis. 


714  Diseases  of  the  Heart. 

My  observations  are  not  sufficiently  large  to  enable  me  to 
draw  any  exact  statistical  conclusions  on  this  point,  but  I  have 
been  very  forcibly  struck  with  the  large  proportion  of  cases  in 
which  the  pericardium  is  found  to  be  adherent  after  death. 
The  symptoms  and  signs  of  pericarditis  are  met  with  in  the 
course  of  some  aneurisms  during  life  ;  and  so  satisfied  am  I 
of  the  frequency  with  which  pericarditis  is  produced  by  the 
pressure  of  an  aneurismal  sac,  that  in  any  case  of  non- 
rheumatic  pericarditis  occurring  after  the  age  of  forty,  in 
which  the  cause  of  the  pericarditis  is  obscure,  I  strongly 
suspect  the  presence  of  an  aneurism.  (In  many  cases  in 
which  the  symptoms  of  angina  pectoris  are  associated  with 
the  physical  signs  of  pericarditis,  and  in  which  the  cause  of 
the  pericardial  inflammation  is  obscure,  as  for  example  in  the 
case  recorded  on  page  310,  the  primary  lesion  is,  I  believe, 
an  aneurism  of  the  root  of  the  aorta.) 

Compression  of  the  piilinoiiary  artery. — An  aneurism  of  the 
root  of  the  aorta  may  compress  the  pulmonary  artery  and  pro- 
duce a  systolic  pulmonary  murmur.  It  seldom  happens  that  the 
compression  is  sufficiently  great  to  produce  much  obstruction 
to  the  blood  flow,  and  (consequent)  venous  engorgement. 

Compression  of  the  left  auricle  is  not  unfrequently  produced 
by  an  aneurism  of  the  root  of  the  aorta,  but  the  compression 
is  seldom  sufficiently  great  to  impede  the  blood  flow  through 
the  pulmonary  circuit. 

Compressioii  of  the  inferior  eava,  or  of  the  left  innominate 
vein  is  not  uncommon,  and  is  of  course  most  apt  to  arise 
when  the  ascending  or  transverse  portions  of  the  aortic  arch 
are  affected.  As  the  result  of  the  compression,  the  return 
current  of  blood  from  the  head  and  neck,  upper  extremities, 
and  upper  surface  of  the  chest  (through  the  internal  mammary 
veins)  is  interfered  with  ;  the  external  jugular  and  other  veins, 
which  discharge  into  the  vena  cava,  become  distended,  and 
subcutaneous  dropsy,  swelling  of  the  face  and  the  other  con- 
ditions, which  have  been  previously  described,  ultimately  may 
occur.  In  some  cases,  the  pressure  of  the  aneurism  produces 
inflammation  of  the  venous  coats  ;  the  vein  may  then  become 
plugged,  and    may  be  felt   as   a  dense   firm   cord,  which,   in 


Physical  Signs  of  Thoracic  Aneurism.         715 

some  cases  {i.e.  in  the  earlier  stages  of  the  condition)  is  tender 
to  the  touch.  In  a  few  cases,  the  aneurism  ruptures  with  the 
vein,  and  an  arterio-venous  murmur  is  estabhshed.  It  is 
important  to  remember,  as  I  shall  afterwards  point  out  in 
speaking  of  the  diagnosis,  that  aneurismal  tumours  are  less 
likely  to  produce  obstruction  of  the  venous  return  than  solid 
intra-thoracic  growths, 

B.  Forzvard  effects.  —  In  many  cases  of  intra-thoracic 
aneurism  (more  especially  when  the  aneurismal  sac  is  situ- 
ated between  the  heart  and  the  origin  of  the  great  blood- 
vessels which  arise  from  the  transverse  portion  of  the  aortic 
arch,  or  when  these  vessels  are  themselves  implicated  or 
pressed  upon  by  the  aneurismal  sac),  the  pulse  in  the  arteries 
on  the  peripheral  side  of  the  sac  is  materially  altered.  These 
alterations,  which  constitute  one  of  the  most  important  second- 
ary or  indirect  physical  signs  of  the  disease,  are  in  some  cases 
due  to  the  fact  that  the  blood  wave,  as  it  passes  through  the 
sac  of  the  aneurism,  is  modified  ;  in  others  to  the  circum- 
stance, that  the  aneurismal  sac  presses  upon  and  obstructs 
one  or  other  of  the  vessels  (innominate,  left  common  carotid, 
or  left  subclavian)  which  spring  from  the  aortic  arch.  Altera- 
tions in  the  peripheral  arteries  are  usually  best  observed 
in  the  radial  arteries  ;  but  the  condition  of  the  carotid  and 
femoral  pulse  should  also  be  noted. 

The  pulse  wave  (or  rather  the  period  of  maximum  impulse 
of  the  pulse  wave)  is  retarded,  and  the  curves  of  the  pulse 
wave  are,  as  it  were,  flattened  out  or  effaced.  In  well-marked 
cases,  the  up-stroke  of  the  sphygmographic  tracing  is  sloping, 
the  apex  rounded,  and  the  secondary  curves  more  or  less  or 
entirely  obliterated.  These  alterations  are  best  marked  when 
the  aneurismal  dilatation  is  globular,  and  when  the  walls  of 
the  sac  are  elasti'c.     (See  figs.  275,  276,  277,  and  278.) 

The  retardation  of  the  pulse  is  best  appreciated  by  the 
finger  ;  the  obliteration  of  the  pulse  curves  by  means  of  the 
sphygmograph. 

Differences  in  the  pulse  tracings  from  the  two  wrists  are 
not  observed  in  all  aneurisms.  When  the  arch  of  the  aorta, 
below  the  origin  of  the  innominate  is  involved,  the  pulse  wave 


7 1 6  Diseases  of  tlie  Heart. 

in  the  two  wrists  is  the  same/  though  the  sphygmographic 
tracing  on  each  side  may  be  modified,  each  pulse  wave  being 


Pressure  3  oz. 
Fig.   2-j$.—Aiteiinsin  of  Left  Axillary  Artery  (left  radial  tracing).— \..  G.,  cet. 
63,   admitted  to  the  Newcastle   Infirmary  7th  March   1878,   with  a  large 
aneurism  of  the  left  axillary  artery.     The  apex  is  rounded ;  all  the  curves 
are  obliterated. 


Pressure  3  oz. 
Fig.  276. — Aneurism  of  Left  Axillary  Artery  (right  radial). — Right  radial  tracing 
for  the  same  [)atient.     The  pulse  is  intermittent,  but  all  the  curves  are  well 
marked. 


Fig.  277. — (Left  radial).  Pressure  },0'..  Fig.  27S. — (Right  radial).  Pressure  t^^oz. 
P'iGS.   277  and  278. — Aneurism  of  Left  Subclavian. — ^J.  M.,  set.  50,  admitted  to 

Newcastle  Infirmary  5th  September  1878  ;  all  the  waves  in  the  left  tracing 

are  obliterated. 

affected,  quoad  its  curves  in  a  Hke  degree.  (See  figs.  279  and 
280.)  When  the  aneurismal  sac  involves  the  innominate,  the 
left  subclavian  being  unaffected,  the  right  radial  pulse  is 
modified,  while  the  left  is  normal.  When  the  sac  is  situated 
between  the  origin  of  the  innominate  and  left  subclavian,  or 
when  the  left  subclavian  is  implicated  (the  circulation  through 
the  innominate  being  uninterfered  with),  the  right  radial  pulse 
is   normal   but   the   left   may  be   modified.     (Further  details 

'  An  exception  to  this  statement  occurs,  when  an  aneurism  of  the  ascending 
portion  of  the  aortic  arch  presses  upon  or  displaces  the  innominate  artery  so  as  to 
interfere  with  the  free  passage  of  the  blood  through  that  vessel,  without  pressing 
upon  or  interfering  with  the  passage  of  the  blood  current  through  the  left  sub- 
clavian arterv. 


Physical  Signs  of  Tluracic  Ancurisiu.         717 

have    previously   been    given    in    treating    of   the    pulse    and 
sphygmograph,  see  p.  283.) 


Fig.  279. — (Right  radial.)  Pressure  ^oz.     Fig.  2S0. — (Left  radial.)  Pressure  \  0-. 

Figs.  279  and  280. — Aneurism  of  Ascendijig portion  of  Aortic  Arch. — J.  D.,  aet. 
50,  admitted  to  Newcastle  Infirmary  suffering  from  a  large  aneurism  of  the 
ascending  thoracic  aorta  and  atheroma.  There  is  no  important  difference 
between  the  two  pulses. 

Embolic  syviptovis  sometimes  arise  from  portions  of  fibrine 

being  washed  away  from  the  aneurismal  sac  and  carried  to  some 

distant  vessel.    This  accident  is  of  less  frequent  occurrence  than 

might   theoretically  be  supposed.     The  exact   nature  of  the 

symptoms  depends,  of  course,  upon  the  vessel  which  happens  to 

be  obstructed  and  the  function  of  the  part  which  it  supplies. 

Physical  sig)is  due  to  altered  condition   of  organs  and  parts 
other  than  the  heart,  arteries,  and  veins. 

The  secondary  physical  signs,  which  result  from  the  pres- 
sure of  the  aneurismal  sac  upon  the  organs  and  parts  which 
surround  it,  are  both  numerous  and  important.  Some  of 
them  have  already  been  incidentally  mentioned  in  speaking 
of  the  ^pressure  syuiptonisl 

When  the  aneurismal  sac  presses  on  the  right  bronchus, 
and  interferes  with  the  free  entrance  of  air  into  the  right  lung, 
the  respiratory  murmur  is  fainter  on  the  right  side  than  on 
the  left,  the  percussion  note  over  the  right  side  of  the  chest  is 
usually  impaired  and  raised  in  pitch,  and  a  wheezing,  whistling 
sound  is,  in  some  cases,  heard  over  the  position  of  the  com- 
pressed tube.  Pressure  on  the  main  bronchus  of  the  left  side, 
is  accompanied  by  corresponding  alterations  in  the  left  lung. 

Pressure  on  the  root  of  the  Ittng,  more  especially,  it  is  sup- 
posed, on  the  braJiehes  of  the  pulmonary  plexus  of  nerves,  is 
occasionally  followed  by  destructive  inflammation  of  the  lung 
tissue.  In  some  of  these  cases  the  lung  is  found  collapsed 
after   death,  and   studded   with  small    abscesses.      In   a  case. 


7i8  Diseases  of  the  Heart. 

which  has  quite  recently  come  under  my  observation  in  the 
post-niortcvi  theatre,  the  lower  lobe  of  the  left  lung  was 
consolidated  and  riddled  with  cavities,  the  result  of  the 
pressure  of  the  sac  of  a  large  aneurism  ;  haemoptysis,  which 
ultimately  proved  fatal,  was  caused  b}^  the  rupture  of  the  sac 
into  one  of  these  cavities  ;  the  upper  lobe  of  the  left  lung,  and 
the  right  lung  were,  with  the  exception  of  emphysema,  per- 
fectly healthy.  In  cases  of  this  description,  the  physical  signs 
of  collapse,  or  breaking  down  of  the  lung,  may  sometimes  be 
obsen'ed  during  life.  Pressure  on  the  trachea  is,  in  many 
cases,  attended,  as  has  been  previously  remarked,  by  stridor. 

On  auscultating  the  trachea,  a  blowing  murmur,  synchronous 
with  the  action  of  the  heart,  can  be  heard  in  some  cases  of  aneur- 
ism, as  Dr  D.  Drummond  has  pointed  out.  It  seems  to  be  an 
exaggeration  of  the  shock,  which  is  usually  communicated  to  the 
air  in  the  chest  by  the  expansion  and  contraction  of  the  heart. 

Pressure  on  the  left  recurrent  laryngeal  nerve  often  produces 
paralysis  or  spasm  of  the  left  vocal  cord,  conditions  which 
can,  of  course,  be  readily  recognised  by  the  laryngoscope. 

Pressure  on  the  oesophagus  produces  dysphagia,  which  may 
be  demonstrated  by  making  the  patient  swallow  a  piece  of 
solid  food,  and  by  observing  the  result,  and  by  auscultating 
the  oesophagus  during  the  act  of  sw^allowing  solid  and  liquid 
substances.  An  oesophageal  bougie  must  not  be  passed  in 
cases  of  this  description. 

Pressure  upon  the  fibres  of  the  sympathetic,  more  especially 
those  fibres  which  are  connected  with  the  lower  cervical  and 
first  dorsal  ganglia,  produces  alterations  in  the  size  of  the  pupil 
and  in  the  vaso-motor  condition  of  the  head  and  neck.  These 
alterations  are  usually  restricted  to  one  side,  since,  as  a  rule, 
the  nerves  on  one  side  only  are  implicated.  The  exact  nature 
of  the  pupil  and  vaso-motor  modifications  depends  upon  the 
manner  in  which  the  sympathetic  fibres  are  affected.  Irrita- 
tion of  the  cilio-spinal  branches  of  the  sympathetic  on  one 
side  produces — {a)  spasm  of  the  dilator  muscle  of  the  pupil 
(which  is  supplied  by  the  sympathetic),  and  [U)  contraction 
of  the  blood  vessels  of  the  corresponding  side  of  the  head  and 
neck,  manifested  externally  by  pallor  and  dryness  of  the  skin 


Physical  Signs  of  TJioracic  Anciirisiu.         719 

and  diminution  of  temperature.  Destriictioii  of  the  cilio-spinal 
branches  of  the  sympathetic,  causes  {a)  paralysis  of  the  dilator 
muscle  of  the  iris  and  contraction  of  the  pupil  (in  consequence 
of  unopposed  action  of  the  pupil  sphincter,  which  is  supplied 
by  the  third  nerve),  and  [b)  dilatation  of  the  blood  vessels  of 
the  head  and  neck  on  the  affected  side,  conditions  which  are 
manifested  externally  by  congestion,  elevation  of  temperature, 
and  unilateral  sweating.^  Too  much  importance  must  not, 
however,  be  attached  to  differences  in  the  size  of  the  pupil,  for 
inequality  in  the  size  of  the  pupils  is  of  frequent  occurrence 
even  in  health,  and  may  be  due  to  many  different  pathological 
conditions.  When  combined  with  an  altered  vaso-motor  con- 
dition of  the  side  of  the  head  and  neck,  inequality  in  the  size 
of  the  pupils  is  only  suggestive  of  intra-thoracic  pressure  ; 
and  even  when  it  is  proved  to  be  the  result  of  intra-thoracic 
pressure,  it  does  not  necessarily  follow  that  an  aneurism  is  the 
cause  of  that  pressure,  for  the  pressure  may  be  due  to  a  solid 
intra-thoracic  growth. 

Dozvnward  displacement  of  the  liver  is  observed  in  some 
cases  in  which  the  thoracic  aneurism  is  of  large  size. 

Summary  of  the  Chief  Symptoms  and  Physical  Signs  zvhich 
are  met  zvith  in  Aneurisms  of  the  different  parts  of  the 
Thoracic  Aorta. 

In  order  to  complete  this  description,  it  may  perhaps  be  well 
to  sum  up  the  ^///(/"symptoms  and  physical  signs,  which  result 
from  aneurisms  of  the  root  of  the  aorta,  and  of  the  ascending, 
transverse,  and  descending  portions  of  the  vessel  respectively. 

'  '  This  dilating  influence  of  the  sympathetic  may,  as  in  the  case  of  the  vaso- 
motor action  of  the  same  nerve,  be  traced  back  down  the  neck,  along  the  rami 
communicantes  and  roots  of  the  last  cervical  and  first  dorsal  or  two  first  dorsal 
spinal  nerves,  to  a  region  in  the  lower  cervical  and  upper  dorsal  cord  (called  by 
Budge  the  centrum  cilio-spinale  inferius),  and  from  thence  up  through  the  medulla 
oblongata  to  a  centre,  which,  according  to  Henson  and  Volckers,  lies  in  the  floor 
of  the  front  part  of  the  aqueduct  of  Sylvius.' — [A  Text-Book  of  Physiology,  by 
Professor  Michael  Foster,  p.  466,  third  edition.)  Professor  Ferrier  tells  me  that 
his  observations  show  that  the  dilating  fibres  pass  out  of  the  spinal  cord  through 
the  anterior  root  of  the  second,  and  perhaps  in  some  cases  of  the  first,  dorsal 
nerves.  I  have  not  been  able  to  find  the  paper  to  which  Professor  Ferrier  referred 
me,  in  the  Philosophical  Transactions. 


720  Diseases  oj  the  Heart. 

1.  Ancurisui  of  the  root  of  tJic  aorta  involving  tJic  sinuses 
of  Valsalva. —  In  cases  of  this  description,  the  aneurism  is 
often  entirely  latent,  i.e.  it  may  give  rise  to  no  symptoms,  and 
may  not  be  attended  with  any  distinct  signs.  Incompetence 
of  the  aortic  valves  is  often  present.  In  some  cases,  attacks  of 
angina  pectoris  (due  to  irritation  of  the  branches  of  the  car- 
diac plexus)  are  obscr\-ed.  Pericarditis  is  frequently  produced 
by  the  irritative  pressure  of  the  sac,  and  is  a  highly  satisfactory 
result,  for,  in  consequence  of  the  adhesions,  the  aneurism  is 
unable  to  rupture  into  the  sac  of  the  pericardium — a  common 
termination  of  aneurisms  in  this  situation,  in  those  cases  in 
which  the  pericardium  is  unadherent.  In  rare  and  exceptional 
cases  the  aneurism  may  burst  into  the  pulmonary  artery,  or 
into  the  left  auricle  of  the  heart  (see  fig.  281).  Aneurisms  of 
the  sinuses  of  Valsalva  rarely  attain  to  any  size  ;  the  case 
represented  in  figures  2S2,  283,  284,  285,  and  286,  is,  so  far  as 
I  know,  quite  unique.  Should  the  aneurism  spring  from  the 
anterior  surface  of  the  aorta,  it  may  compress  the  pulmonary 
artery,  and  possibly  give  rise  to  symptoms  and  physical  signs 
of  pulmonary  constriction. 

2.  Aneurisms  of  the  ascending  portion  of  aortic  arch,  above 
tlie  sinuses  of  Valsalva. — This  is  the  part  of  the  thoracic  aorta 
which  is  most  frequently  affected — the  '  seat  of  election'  of  aortic 
aneurisms,  as  I  am  in  the  habit  of  terming  it.  The  aneurism 
usually  makes  its  way  forwards,  and  soon  comes  in  contact 
with  the  front  wall  of  the  chest ;  it  is  often  of  large  size,  and  is, 
as  a  rule;  very  readily  detected  on  physical  examination.  The 
chief  pressure  signs  and  symptoms  to  which  it  gives  rise,  arc 
(a)  pain  ;  {b)  dyspnoea,  cough,  and  alterations  in  the  right  lung 
from  pressure  on  the  pulmonary  tissue  or  right  bronchus  ;  and 
in  some  cases  {c)  engorgement  of  the  veins  of  the  head  and 
neck  from  pressure  on  the  superior  vena  cava.  Aneurisms  in 
this  situation  often  erode  the  front  wall  of  the  chest. 

3.  Aneurisms  of  the  transverse  portion  of  the  aortic  arch 
are  very  common,  though  not  so  common  as  aneurisms  of 
the  ascending  portion.  The  symptoms  and  signs  are,  as  a 
rule,  well  marked  and  characteristic,  and  the  diagnosis  easy. 
The    tumour    sometimes    makes    its    way  up    into    the    neck 


Fig.  281. —  Aneurism  of  the  commencement  of  the  aorta  rupturing  into  the  left  auricle.    (Natural  size.") 

The  left  auricle  and  left  ventricle  have  been  cut  open  from  behind,  a  bridge  of  muscular 
tissue  (6)  being  left  between  them. 

The  letter  a  points  to  three  projections  which  the  aneurism  has  formed  in  the  anterior  wall 
of  the  auricle;  6,  to  a  commimication  between  the  snc  of  the  aneurism  and  the  cavity  of  the 
auricle. 

(The  specimen  is  in  the  Anatomical  Museum  of  the  Edinburgh  University,  and  is  repre- 
sented by  Professor  Turner's  permission.) 


Pig.  282,    Portrait  of  J.  S.,  showing  the  position  and  size  of  the  External  Tumour  when  i 
first  came  under  observation.     (Seen  from  the  right  side.) 


!  patient     i 


Fig.  283.    Portrait  of  J.  S.,  shmeing  Vie  position  and  size  of  the  External  Tumour  when  the  patient 
first  came  und^r  observation,    (Front  view.) 


M'L«4Hl&j»«i««ljt«c'Ei>i 


FiQ.  284.    Sternum  and  adjacent  ribs,  shmoing  the  apertures  of  perforation ,  and  the  outline  of  the  base 
of  tlie  false  Anewism  formed  externally  in  the  case  of  J.  3. 

The  letter  a  points  to  the  terminatiou  of  the  transverse  portion  of  the  aortic  arch ;  b,  to  the 
innominate  artery ;  c,  to  the  manubrium  sterni ;  d,  to  the  ensiform  cartilage ;  e,  e,  e,  e,  to  the 
outline  of  the  base  of  the  false  aneurism ;  g,  g,  to  the  eroded  apertures  in  the  chest  walL 


tiFl».NtC.<»>imoLinic;Eei 


Fio.  285.     Aneurism  springing  from  the  very  commencement  of  the  Aortic  Arch,  and  causing  erosion  of 
Quest  Wall  and  death  hy  external  rupture.    Seen  from  behind.    (jCase  of  J.  S.) 

A  probe  has  been  passed  into  the  aortic  orifice  ;  the  left  ventricle  has  been  cut  away,  and  the 
interior  of  the  right  ventricle  exposed.  The  sac  of  the  aneurism  is  seen  to  be  in  close  contact 
with  the  exterior  of  the  right  auricle,  right  ventricle,  and  pulmonary  artery. 

The  letter  a  points  to  the  aneurism  at  its  point  of  origin  at  the  root  of  the  aorta  ;  b,  b,  b,  to 
the  secondary  tumours  which  it  has  formed,  and  which  are  in  contact  with  the  chest  wall ;  c,  to 
the  orifice  of  the  pulmonary  artery ;  d,  to  the  aortic  arch  above  the  aneurismal  sac ;  e,  to  the 
interior  of  the  right  ventricle. 


MH«u>iiCuiin<«c.ljT<ic!  Eota! 


Fig.  286.  Aneurism  springing  from  the  commencement  of  the  Aortic  Arch,  and  causing  erosion  of  the 
Chest  Wall  in  the  Lower  Sternal  Region,  and  eventually  producing  the  large  external  tumour 
represented  in  figs.  282  and  283.  {The  aneurism  and  the  bony  wall  of  the  Thorax,  as  seen  from  the 
right  side.) 

The  letter  a  points  to  the  ascending  portion  of  the  arch  of  the  aorta,  from  the  commencement 
of  which  the  aneurism  6  springs ;  f,  the  innominate  artery;  m,  the  manubrium  sterni;  d,d,  the 
base  of  the  external  tumour;  e,  the  ensiform  cartilage. 


M'UMMilUaxxic.bnoUo 


Fig.  287.  Anmiism  of  tlie  transverse  portion  of  the  Aortic  Arch,  wldch  produced  great  difficulty  in 
breathing  from  pressure  upon  the  Trachea  and  Left  Recurrent  Laryngeal  neree.  Death  resulted 
from  rupture  into  the  Trachea.    (Front  view,  natural  size.') 

The  letter  a,  poiuts  to  the  ascending  portion  of  the  aortic  arch ;  b,  to  the  innominate  artery; 
c,  to  the  left  common  carotid  artery ;  d.  to  the  left  subclavian ;  c,  to  the  descending  portion  of 
the  aortic  arch ;  /,  to  the  pulmonary  artery ;  g,  to  the  oesophagus ;  h,  to  the  left  pneumogastric 
nerve. 


Fig.  288.  Aneurism,  of  the  transverse  portion  of  the  Aortic  Arch,  which  produced  great  difficulty  in 
breathing  from  pressure  upmi  the  Trachea  and  left  Recurrent  Laryngeal  Nerve.  Decdh  resulted 
from  rupture  into  the  Trachea.     {Back  view,  natural  size.') 

The  letter  a  points  to  the  ascending  portion  of  the  aortic  arch;  h,  to  the  innominate  artery; 
c,  to  the  left  common  carotid  artery;  </,  to  the  left  subclavian;  c,  to  the  descending  portion  of 
the  aortic  arch ;  /,  to  the  pulmonary  artery ;  h,  to  the  oesophagus ;  i,  to  the  aperture  of  rupturo 
in  the  trachea,  which  is  situated  immediately  above  the  bifurcation  of  the  bronchi. 


Fig.  289. — Aneurism  of  tlve  thoracic  aorta,  rupturing  into  the  oesoptiagus.    (Natural  size,  seen  from 

behind!) 

The  letter  a, points  to  the  oesophagus  just  above  the  orifice;  6,  to  the  aneurism.  The  sac  was 
almost  completely  filled  with  laminated  tibrine,  the  clot  can  be  seen  through  the  orifice  in  the 
oesophagus. 


MH.s.™lC<>K«i«i;.liTHc'  Eoi 


Fig.  290. — Erosion  of  the  spinal  column  due  to  the  pressvre  of  an  aneurism.     (^Natural  size.') 

The  anterior  surface  of  the  bodies  of  two  vertebras  are  extensively  destroyed,  and  the  spinal 
canal  is  exposed. 


MH.rj.JCgnuiNoLiTnoUDi 


Fig,  292. 


Fig.  294 


Fig.  293 


Fig.  291. 


Fig.  291.     Clotfnm.  the  interior  of  a  large  aneurism  oftlie  Innominate  arUry.    (Natural  size.) 


FiQ.  292. Laminated  blood  clot  from  an  aneurism  of  the  popliteal  artery  in  a  boy  icho 

suffered  from  cardiac  disease.     (Natural  size,') 

The  aneurism  had  undergone  a  spontaneous  cure  ;  the  lamination  of  the  clot  is 
well  shown. 

Figs.  293  and  294. —  Clots  from  aneurisms  of  the  innominate  and  left  con<,mon  carotid 
arteries.    (Natural  size). 


A  narrow  channel,  a,  a',  passes  through  the  centre  of  each  clot. 


MHas.i>*Cv— it.sLiT«o'Eo.N 


Symptoms  and  Signs  of  Thoracic  A  neurisms.     7 2 1 

(see  fig.  2^^^  ;  its  pulsation  can  usually  be  felt  in  the  supra- 
sternal notch  ;  alterations  in  the  characters  of  the  two  radial 
or  the  two  carotid  pulses  are  frequently  observed,  for  one  or 
other  of  the  large  branches  springing  from  the  arch  is  often 
implicated  in  the  sac  or  obstructed.  The  oesophagus,  trachea, 
recurrent  laryngeal  nerve,  and  the  left  innominate  vein  are 
the  parts  which  are  most  liable  to  be  pressed  upon.  The 
aneurism  often  proves  fatal  by  rupturing  into  the  trachea  or 
oesophagus.     (See  figs.  288  and  289.) 

4.  Aneurisms  of  tJie  descending  portion  of  the  thoracic 
arch  and  of  the  descending  thoracic  aorta  are  often  latent, 
and  until  they  have  perforated  the  chest  wall  (which  they 
sometimes  do)  they  are  very  difficult  to  detect  by  means  of 
physical  examination.  A  dull,  boring,  localised  pain  in  the 
back  or  spinal  column  is  very  generally  present,  and  is 
highly  characteristic.  The  oesophagus  and  root  of  the  left 
lung  are  very  likely  to  be  pressed  upon.  The  thoracic  duct 
and  azygos  vein  are  often  also  implicated.  A  systolic  mur- 
mur over  the  seat  of  the  pain  in  the  back  is  highly  sugges- 
tive. Aneurisms  of  this  part  of  the  aorta  often  rupture 
into  the  left  pleura,  or  into  the  oesophagus  (see  fig.  289)  ; 
they  very  frequently  erode  the  bodies  of  the  vertebrae  (see 
fig.  290^),  and  may  finally  press  upon  the  spinal  cord,  or  burst 
into  the  spinal  canal.  In  some  cases  they  perforate  the  chest 
wall,  usually  to  the  left  side  of  the  spinal  column. 

Course  and  terminations. — The  average  duration  of  aneu- 
risms of  the  thoracic  aorta  is  said  to  be  about  two  years  from 
the  time  when  the  condition  is  first  recognised  ;  but  the  course 
and  duration  are  very  uncertain,  for,  on  the  one  hand,  the  con- 
dition may  at  any  moment  prove  fatal,  and  on  the  other,  cases 
have  been  met  with,  in  which  the  subjects  of  thoracic  aneurism 
have  for  years  been  able  to  follow  their  ordinary  occupations 
without  any  very  great  inconvenience."'     The  termination  is 

'   In  this  case  the  aneurism  involved  the  abdominal  aorta. 

-  Balfour  relates  a  case  in  which  the  patient  maintained  himself  for  ten  years 
as  a  hotel  porter,  with  a  large  aneurism  projecting  through  the  walls  of  the  chest. 
—Diseases  of  the  Heart,  p.  405. 

Z    Z 


72  2  Diseases  of  the  Heart. 

almost  invariably  fatal.  In  extremely  rare  cases,  the  aneurism 
consolidates  and  is  cured.  Death  is  generally  caused  by 
rupture  of  the  sac.  The  aneurism  may  burst  into  the  pleura, 
lung  tissue,  trachea,  bronchi,  cesophagus,  pericardium,  through 
the  diaphragm,  or  externally.  In  a  minority  of  cases  death  is 
due  to  gradual  and  progressive  exhaustion  and  inanition,  or  to 
some  inter-current  complication. 

Diagnosis. — The  steps  in  the  diagnosis  of  a  supposed  case 
of  aneurism  of  the  thoracic  aorta  are  : — 

1.  Is  a  thoracic  aneurism  present  ? 

2.  If  a  thoracic  aneurism  is  present,  is  it  an  aneurism  of 
the  thoracic  aorta .'' 

Step  No.  I .  Is  a  thcracic  aneurism  present  ? 
This  question  is  in  some  cases  decided  with  the  greatest 
ease,  in  others,  the  diagnosis  is  difficult  or  impossible.  When 
the  aneurism  is  small  and  deep  seated,  and  when  there  are 
no  pressure  symptoms,  the  diagnosis  is  impossible.  Many 
aneurisms  of  the  sinuses  of  Valsalva  come  under  this  head. 
In  cases  of  this  description,  the  aneurism  may  burst  into  the 
pericardium  and  suddenly  cause  the  death  of  a  patient  who 
had  previously  made  no  complaints,  and  who  had  presented 
up  to  the  time  of  death  all  the  appearance  of  robust  health. 
The  case  from  which  the  specimen  represented  in  fig.  270  was 
drawn,  is  an  excellent  illustration  in  point.  When,  on  the 
other  hand,  the  aneurism  has  perforated  the  chest  wall,  and 
formed  an  external  pulsating  tumour,  the  diagnosis  is  self- 
evident.  When  the  aneurism  is  large,  and  more  especially 
when  it  is  in  contact  with  the  chest  wall  (even  although  it 
has  not  perforated),  the  diagnosis  is  generally  easy. 

The  physical  signs  which  are  of  greatest  importance  from 
a  diagnostic  point  of  view  are — (i)  a  circumscribed  dull  area 
in  the  course  of  the  aorta  ;  (2)  pulsation  over  the  dull  area, 
more  especially  pulsation  of  an  expansile  character,  syn- 
chronous with  the  cardiac  systole,  and  at  least  as  forcible  as 
the  pulsation  of  the  heart ;  (3)  well  marked  auscultatory 
phenomena,   more    particularl}'   a    s\\stolic    murmur    with    an 


Diagnosis  of  Anenrisin  of  the  Thoracic  Aorta.  723 

accentuated  second  sound,  or  an  accentuated  second  sound 
with  a  normal,  feeble  or  toneless  first  sound,  over  the  dull 
area ;  and  (4)  pain  and  other  pressure  symptoms.  When 
these  symptoms  and  signs  are  met  with  in  combination,  the 
diagnosis  does  not  present  any  difficulty.  Difficulties  in 
diagnosis  chiefly  arise  in  those  cases  in  which  some  only  of 
the  physical  signs  just  mentioned  are  present. 

The  conditions  which  are  most  likely  to  be  confounded 
with  aneurisms  of  the  thoracic  aorta  may  be  conveniently 
divided  into  two  groups,  viz. : — 

Group  I.  Conditions  in  whic/i  some  of  tJie  pJiysical  signs  of 
t]i07'acic  ane7irisms  {inorc  cspccialty  tocalised  dutness  on  percussion 
a)id pulsation  in  tlie  course  of  the  aorta)  aj-e  present,  but  in  whicJt 
thej'e  are  no  pressure  signs. 

Group  2.  Cases  in  ivJiich  there  ai'e  pressure  signs,  together 
ivith  some  of  the  pJiysical  signs  of  thoracic  aneurism. 

The  chief  conditions  included  under  these  groups  (which 
run  into  each  other)  are  : — 

I.  Simple  dynamic  pulsation  of  tJie  thoracic  aorta. — This  is 
certainly  a  rare  condition — infinitely  more  rare  than  simple 
dynamic  pulsation  of  the  abdominal  aorta,  which  is  not 
unfrequently  mistaken  for  an  aneurism  of  the  abdominal 
aorta — but  it  does  occasionally  occur.  It  was  probably  the 
cause  of  very  distinct  pulsation,  and  some  dulness  in  the 
second  right  interspace,  in  a  case  which  I  saw  recently 
in  consultation  with  Dr  William  Murray  of  Newcastle-on- 
Tyne. 

The  patient,  a  very  robust  and  healthy-looking  young 
man,  came  under  Dr  Murray's  care,  complaining  of  palpita- 
tion, and  a  feeling  of  uneasiness  in  the  region  of  the  heart  ; 
pain  and  pressure  symptoms  were  entirely  absent,  but  pulsa- 
tion and  dulness  over  the  aorta  were  so  distinct  as  to  lead  Dr 
Murray — whose  diagnostic  ability  generally,  and  in  aneurism 
in  particular,  is  well  known— to  believe  that  an  aneurism  of 
the  ascending  portion  of  the  aortic  arch  was  probably  present. 
After  some  months  of  treatment,  the  local  indications  of 
aneurism  gradually  subsided,  and  when  I  saw  the  case  they 
had    completely    disappeared.      The    pulse    throughout    the 


724  Diseases  of  the  Heart. 

course  of  the  attack,  and  at  the  time  of  my  visit,  was  un- 
duly slow,  but  there  were  no  physical  signs  of  organic 
cardiac  disease.  So  far  as  Dr  Murray  and  I  could  judge, 
the  condition  was  probably  neurotic.  In  these  cases  the 
absence  of  pain  and  other  pressure  signs  is  a  point  of  cardinal 
importance.  The  fact  that  there  is  no  evidence  of  organic 
disease  of  the  heart  and  arteries  ;  the  age  and  sex  of  the 
patient  (neurotic  pulsation  being  almost  exclusively  con- 
fined to  young  adults,  and  being  much  more  common  in 
women  than  in  men)  ;  and  the  presence  of  symptoms 
and  signs  indicative  of  deranged  cardiac  innervation,  such, 
for  example,  as  an  uneasy  feeling  in  the  region  of  the 
heart,  consciousness  of  the  heart's  action,  and  palpitation, 
are  the  points  on  which  reliance  must  be  placed  in  making 
the  diagnosis. 

2.  Displaceuient  of  the  aorta  the  result  of  spinal  curvature. — ■ 
Curvature  of  the  spine  not  unfrequently  displaces  the  aorta 
forwards  and  to  the  right.  Some  pulsation  and  dulness  may 
be  present  in  the  second  right  interspace,  and  may  lead  to 
the  supposition  of  aortic  aneurism.  When  the  patient  is  in 
good  health,  more  especially  when  the  heart  and  arteries 
are  healthy,  the  diagnosis  does  not  present  much  difficulty. 
Great  importance  is  to  be  attached  to  the  absence  of  pain 
and  other  symptoms  of  intra-thoracic  pressure.  In  those 
cases  in  which  the  heart  is  diseased,  the  diagnosis  may  be 
most  difficult,  and  so  far  as  my  experience  enables  me  to 
form  an  opinion,  disease  of  the  heart  and  of  the  aorta  is  of 
frequent  occurrence  in  those  cases  in  which  the  upper  outlet 
of  the  thorax  is  narrower  than  normal. 

The  following  case,  which  I  reported  some  years  ago  in 
the  Lancet  (March  9th,  1878,  page  346),  illustrates  the  diffi- 
culties in  diagnosis  in  some  cases  of  this  description. 

Case. — Malposition  of  the  Aorta  due  to  Rickets.,  simulating  Aneurism 
of  ttie  ArcJi  fJie  Aorta. 

W.  W.,  aet.  46,  an  engineer,  was  admitted  to  the  Newcastle-on-Tyne 
Infirmary  under  my  care,  on  June  loth,  1875,  suffering  from  orthopncea 
and  general  dropsy. 


Diagnosis  of  Anciirisin  of  the  TJioracic  Aorta.  725 

Previous  history. — He  enjoyed  good  health  until  he  was  thirty-five 
years  of  age.  He  was  then  laid  up  with  bronchitis  and  pleurisy.  The 
bronchitis  has  returned  every  now  and  again  since.  The  present  attack 
commenced  three  months  ago  with  cough  and  expectoration.  He  has 
been  confined  to  bed  for  seven  weeks.  Dropsy  set  in  six  weeks  ago. 
His  spine  has  been  very  much  curved  since  he  was  a  little  boy. 

Cojtdition  071  adinissio?!. — There  is  great  general  dropsy.  He  is  very 
short  of  breath.  The  face  and  upper  extremities  are  markedly  cyanotic. 
The  external  jugular  veins  are  distended.  The  root  of  the  neck  looks 
swollen,  and  there  seems  to  be  a  constriction  of  the  upper  part  of  the 
thorax.  The  chest  is  prominent  in  front,  more  so  on  the  left  than  on  the 
right  side.  The  spine  in  the  lower  cervical  and  upper  dorsal  regions  is 
very  much  curved,  the  direction  of  the  curvature  being  forwards  and  to 
the  right.  The  prtecordia  is  prominent.  Dull  heaving  pulsation  is  felt 
all  over  the  prjecordial  area,  and  in  the  second  and  third  intercostal 
spaces  both  to  the  right  and  left  of  the  sternum.  There  is  strong  pulsa- 
tion in  the  supra-sternal  notch.  The  pulsation  is  most  marked  in  the 
second  left  intercostal  space  just  outside  the  sternum.  There  is  marked 
dulness  on  percussion  over  the  manubrium,  and  on  both  sides  of  it  over 
the  area  of  pulsation  described  above.  The  area  of  cardiac  dulness  is 
considerably  increased,  measuring  four  and  a  half  inches  transversely. 
On  auscultation  over  the  manubrium  and  area  of  pulsation  to  the  right 
and  left  of  it,  the  cardiac  sounds  are  heard,  valvular  and  superficial  in 
character,  the  second  being  decidedly  accentuated.  These  characters 
are  most  marked  over  the  area  of  maximum  pulsation  in  the  second  left 
intercostal  space.  At  the  cardiac  apex  the  sounds  are  normal.  The 
radial  pulse  numbers  120;  it  is  regular,  ver}^  much  weaker  in  the  left 
than  in  the  right  wrist.  Respiration  in  the  left  lung  is  weaker  than  in 
the  right.  Bronchitic  rales  are  heard  all  over  the  chest,  and  there  is 
some  dulness  over  the  bases  of  the  lungs  (hydrothorax).  With  the  ex- 
ception of  the  venous  obstruction  already  described,  there  are  no  pressure 
symptoms. 

It  is  unnecessary  to  give  the  daily  progress  of  the  case  ;  suffice  it  to 
say,  that  the  patient  gradually  got  worse,  and  died  on  June  i6th. 

Autopsy  twenty-one  hours  after  death. — The  anterior  curvature  of  the 
spine  was  very  great,  the  distance  between  the  second  right  sterno-costal 
articulation  and  the  spinal  column  being  only  one  inch  and  a  half  All 
the  structures  passing  in  and  out  of  the  superior  outlet  of  the  thorax 
were  compressed.  The  aorta  was  displaced  forwards  and  towards  the 
left.  The  oesophagus  passed  tolerably  freely  along  the  left  side  of  the 
projecting  vertebrae.  The  pericardium  was  universally  adherent,  the 
adhesions  being  recent.  The  heart  weighed  fourteen  ounces  and  a  half 
The  aortic  valve  was  slightly  incompetent,  and  was  covered  with  minute 
vegetations.  The  aortic  arch  was  normal.  The  lungs  presented  the 
ordinary  appearances  seen  in  acute  bronchitis.    There  was  a  considerable 


726  Diseases  of  the  Heai't. 

amount  of  serous  fluid  in  each  pleural  cavity.  There  was  no  apparent 
cause  for  the  inequality  of  the  pulses,  nor  for  the  inequality  of  the 
respiratory  murmur  on  the  two  sides. 

3.  Pulsating  empyema.  —  This  condition  can  usually  be 
distinguished  without  difficulty  after  a  careful  examination  of 
the  case.  The  pulsation  is  less  forcible  than  the  pulsation  of 
the  heart ;  there  are  no  pressure  symptoms  ;  the  dulness  on 
percussion  and  the  pulsation  may  not  lie  in  the  course  of  the 
aorta,  but  even  when  they  are  so  situated,  the  absence  of 
other  indications  of  cardiac  or  arterial  disease  on  the  one 
hand,  and  the  presence  of  constitutional  derangement  and  of 
local  evidence  of  disease  of  the  lung  or  pleura,  on  the  other, 
enable  us  usually,  without  much  difficulty,  to  come  to  a 
correct  conclusion  as  to  the  nature  of  the  case. 

4.  Soliel  intra-thoracic  tumours. — In  some  of  these  cases, 
the  tumour  is  in  contact  with  the  chest  wall  on  the  one  hand, 
and  with  the  aorta  on  the  other  ;  in  others  the  tumour  is 
deeply  situated.  In  the  latter  case,  more  especially,  the 
differential  diagnosis  is  often  extremely  difficult  or  impossible. 

When  the  tumour  is  in  contact  with  the  chest  zvall  on  the 
one  hand  and  the  aorta  on  the  other^  localised  dulness  over 
the  course  of  the  aorta  is  present ;  there  is  often  an  impulse 
communicated  from  the  aorta  over  the  seat  of  the  dulness  ;  a 
systolic  murmur,  due  to  constriction  of  the  aorta  by  the  pres- 
sure of  the  tumour  is  frequently  present,  and  symptoms  and 
signs  of  intra-thoracic  pressure  may  be  prominent.  Obviously, 
therefore,  an  intra-thoracic  aneurism  will,  in  many  cases,  be 
closely  simulated.  A  careful  observer  can,  however,  usually 
come  to  a  correct  conclusion  as  to  the  nature  of  the  case. 
The  dulness  due  to  a  solid  tumour  is  seldom  so  localised  as  it 
usually  is  in  thoracic  aneurisms  ;  the  impulse  is  usually 
slight,  and  never,  so  far  as  I  know,  equals  the  force  of  the 
cardiac  impulse  (as  the  impulse  of  a  thoracic  aneurism  often 
does)  ;  the  chest  wall  is  rarely  if  ever  eroded  by  a  solid 
growth  arising  within  the  thorax  ;  the  systolic  murmur  due 
to  the  pressure  of  a  solid  intra-thoracic  tumour  on  the  aorta  is 
not  usually  accompanied  by  an  accentuated  second  sound,  in 
fact  the  aortic  second  sound  is  gcnerallv  faint  or  absent  at  the 


Diagnosis  of  A  uciiri sin  of  the  Thoracic  Aoria.  727 

seat  of  the  murmur  ;  the  breath  sounds — often  in  the  form 
of  bronchial  or  tubular  breathing — can  generally  be  heard 
over  the  dulness  due  to  a  tumour,  but  are  absent  over  the 
dulness  due  to  an  aneurism  ;  though  pressure  symptoms  are 
prominent,  pain  is  seldom  great  in  cases  of  solid  intra-thoracic 
growth,  indeed,  in  many  cases  there  is  no  pain  throughout 
the  course  of  the  case  ;  constitutional  symptoms  are  generally 
much  more  marked  in  solid  growths.  But  these  and  other 
points  will  be  presently  considered  in  detail. 

In  a  case,  which  I  have  recorded  in  the  British  Medical 
Journal,  vol.  i.,  p.  8,  1877,  the  signs  of  thoracic  aneurism  were 
very  closely  simulated,  but  space  does  not  allow  me  to  give 
the  details. 

Cystic  tumours  are  occasionally,  though  ver}'  rarely,  met 
with  in  the  cavity  of  the  thorax.  In  the  following  case  the 
cyst  was  in  contact  with  the  arch  of  the  aorta,  and  the  physical 
signs  of  aortic  aneurism  were  closely  simulated.  The  reasons 
which  led  me  ultimately  to  exclude  a  true  sacculated  aneu- 
rism are  set  forth  in  the  remarks  attached  to  the  record  of  the 
case. 

Case  of  Cystic  Tmnoiir  in  the  Ajtterior  Afediastini/jn  siuiulating 
Ancicrism. 

A.  C.  Eet.  50,  single,  a  drayman,  formerly  a  soldier,  was  first  admitted 
to  the  Newcastle-on-Tyne  Infirmaiy,  under  my  care,  on  17th  Februar}- 
1876,  suffering  from  acute  albuminuria  of  three  weeks'  duration. 

Twenty  years  previously  he  had  suffered  from  syphilis.  For  several 
years  past  he  had  been  a  hard  drinker. 

On  examining  the  thorax,  visible  and  tangible  pulsation  was  per- 
ceived in  the  second  right  interspace.  A  slight  systolic  thrill  could 
be  felt  when  the  hand  was  placed  over  the  same  spot,  and  there  was 
well-marked  and  limited  percussion  dulness.  A  systolic  murmur  and 
somewhat  accentuated  second  sound  were  heard  on  auscultation.  (The 
thrill,  systolic  murmur,  and  accentuation  of  the  second  sound  were  per- 
haps better  marked  over  the  mid-sternum  at  the  level  of  the  fourth  costal 
cartilage  than  over  the  area  of  pulsation.) 

There  were  no  pressure  signs  ;  it  was  particularly  noted  that  there 
never  had  been  any  pain.  Shortness  of  breath  and  cough  were  com- 
plained of,  but  were  evidently  due  to  the  presence  of  bronchial  catarrh. 

The  heart  was  of  normal  size,  the  apex  being  situated  an  inch  imme- 
diately below  the  left  nipple. 


728  Diseases  of  the  Heart. 

The  diagnosis,  as  regards  the  thoracic  lesion,  \vas  an  aneurism  of  the 
aortic  arch. 

On  6th  April  the  patient  discharged  himself.  The  urine  still  con- 
tained a  trace  of  albumen,  the  physical  signs  at  the  seat  of  the  supposed 
aneurism  being  the  same. 

0)1  J///  October  he  was  again  admitted,  suffering  from  a  relapse  of  the 
renal  dropsy  ;  and  after  remaining  in  hospital  for  a  month  was  again 
discharged.     The  thoracic  physical  signs  were  still  unchanged. 

He  continued  well  until  September  1877,  when  he  began  to  suffer  from 
pain  in  the  region  of  the  stomach  and  from  difficulty  in  swallowing. 

On  14th  November  1877  he  was  re-admitted  under  my  care.  He  was 
now  greatly  emaciated,  his  expression  was  haggard  and  anxious,  and  he 
presented  a  remarkably  cachectic  appearance. 

The  physical  signs  within  the  thorax  were  as  before,  except  that  the 
apex-beat  was  somewhat  elevated,  corresponding  to  the  left  nipple. 

Pain  and  tenderness  on  pressure  were  complained  of  in  the  epigastric 
region,  but  no  tumour  could  be  perceived.  The  epigastric  pain  was 
increased  immediately  after  taking  food.  There  had  been  no  vomiting. 
The  stomach  seemed  of  normal  size.  There  was  marked  dysphagia,  the 
stoppage  being  referred  to  a  point  corresponding  to  the  lower  end  of  the 
sternum. 

The  right  pupil  was  only  half  the  size  of  the  left.  He  complained  of 
numbness  in  the  fingers  of  the  right  hand. 

The  urine  was  copious,  pale,  sp.  gr.  loio.  It  contained  §  albumen, 
and  a  few  granular  and  hyaline  casts. 

I  now  discarded  the  notion  of  a  true  sacculated  aneurism  in  favour  of 
a  general  dilatation  of  the  aortic  arch.  This  opinion  was  based  upon  the 
continued  absence  of  all  pressure  signs — especially  pain — and  the  un- 
altered condition  of  the  physical  signs  at  the  seat  of  pulsation. 

On  2ist  January  the  patient  was  seized  \\\\\\  a  severe  epileptiform 
convulsion,  and  died  twelve  hours  afterwards. 

The  autopsy  was  made  sixteen  hours  after  death.  The  body  was 
much  emaciated.  A  cystic  tumour,  the  size  of  a  hen's  ^g'g,  was  situated 
in  the  anterior  mediastinum,  in  immediate  contact  with  the  ascending, 
and  the  junction  of  the  ascending  and  transverse  portions  of  the  aortic 
arch.  (The  specimen  was  exhibited  to  the  Edinburgh  Medico-Chirurgical 
Society,  May  1878.)  The  anterior  surface  of  the  tumour  was  partly 
covered  by  lung  tissue,  the  uncovered  portion  being  in  contact  with  the 
chest-wall  at  a  point  corresponding  to  the  second  right  interspace.  The 
cyst  contained  a  clear,  watery-looking  fluid  of  neutral  reaction,  and  of 
sp.  gr.  loio.  The  fluid  was  almost  entirely  coagulated  by  heat  and  nitric 
acid.  On  standing,  it  deposited  a  scanty  sediment  containing  a  few 
leucocytes,  but  no  other  formed  elements. 

The  aorta  was  somewhat  dilated  and  atheromatous  at  its  base.  The 
aortic  valves  were  thickened  and  cartilaginous,  but  competent. 


Diagnosis  of  Aneitrism  of  the  Thoracic  Aorta.  729 

The  heart  weighed  13  oz. 

The  stomach  was  filled  with  a  huge  clot  of  black  blood.  A  large 
ragged  malignant  ulcer  surrounded  the  oesophageal  opening.  The  coats 
of  the  stomach  were  very  much  thickened  at  the  seat  of  the  ulcer.  The 
orifice  of  the  oesophagus  was  partly  obstructed  by  the  new  growth.  The 
kidneys  were  in  an  early  stage  of  the  large  white  form  of  Bright's  disease. 

Remarks. — In  the  works  at  my  disposal  I  cannot  find  any  reference 
to  the  occurrence  of  a  simple  serous  cyst  in  the  anterior  mediastinum. 
The  case  is  obviously,  therefore,  of  great  pathological  rarity.  It  is,  how- 
ever, in  its  clinical  aspects  that  it  is  chiefly  interesting  ;  indeed,  I  have 
not,  either  in  reading  or  in  practice,  come  across  any  case  in  which  the 
direct  physical  signs  of  an  aortic  aneurism  were  so  closely  simulated.  The 
pulsation  and  limited  dulness  at  the  '  seat  of  election'  of  aortic  aneurisms 
resulted,  of  course,  from  the  presence  of  the  tumour  and  from  the  way  in 
which  it  was  related  to  the  aortic  arch.  The  accentuated  second  sound 
was  due,  chiefly,  I  think,  to  the  increased  arterial  tension  which  resulted 
from  the  kidney  disease,  partly  to  the  dilated  condition  of  the  aortic  arch. 
The  systolic  murmur  and  thrill  were  evidently  due  to  the  condition  of 
the  aorta. 

hi  those  cases  in  which  the  solid  intra-thoracic  tuuiour  or 
aneurism  is  deeply  situated,  the  physical  signs  are  of  course 
much  more  indistinct ;  in  many  cases  the  diagnosis  is  ex- 
tremely difificult,  and  can  only  be  arrived  at  by  a  judicial 
survey  of  all  the  facts  and  probabilities  of  the  case,  viz.  : — 

(i.)  The  relative  frequency  of  the  two  diseases. 

(2.)  Certain  general  considerations,  such  as  the  age,  sex. 
and  occupation  of  the  patient. 

(3.)  His  hereditary  tendencies. 

(4.)  His  previous  history. 

(5.)  His  present  condition  (general  appearance,  symptoms, 
physical  signs,  associated  diseased  conditions). 

(6.)  The  progress  of  the  case. 

(7.)  The  influence  of  treatment. 

I  will  now  consider  each  of  these  points  in  detail.  My 
remarks  are  based  upon  a  comparison  of  the  cases  of  aneurism 
analysed  by  the  late  Dr  Sibson,  and  recorded  in  his  great 
work  on  Medical  Anatomy  ;  of  the  cases  of  aneurism  tabu- 
lated by  the  late  Dr  Hayden  ;  and  of  all  the  cases  of  primary 
intra-thoracic  cancer  and  lympho-sarcoma  which  I  could  find 
recorded    in    the    Lancet,    British    Medical  Journal,    Medical 


730  Diseases  of  the  Heart. 

Times  and  Gazette,  and  Transactions  of  the  PatJiologieal 
Society  of  London,  during  a  period  of  fifteen  years,  (This 
analysis  was  made  several  years  ago,  and  as  a  few  of  the 
journals  were  missing  from  the  library  of  the  Newcastle-on- 
Tyne  Infirmary  when  I  made  the  search,  and  as  it  is  not 
therefore  strictly  accurate  or  brought  up  to  date,  I  omit  the 
figures  ;  but  the  main  results  may,  I  think,  be  relied  upon.) 

Relative  frequency  of  aneurism  and  tumour. — Aneurism  is 
much  more  frequent  than  tumour.  (My  own  experience  con- 
firms this  statement  very  strongly,  but  it  must  be  remembered 
that  in  the  neighbourhood  of  Newcastle,  in  which  my  experi- 
ence has  been  chiefly  gained,  aneurisms  abound.) 

Age. — Aortic  aneurisms  are  most  frequent  between  the 
ages  of  thirty  and  fifty,  and  are  extremely  rare  before  twenty. 
Intra-thoracic  tumours  (I  have  limited  the  inquiry,  it  must  be 
remembered,  to  cancers  and  lympho-sarcomatous  growths) 
may  occur  at  any  age,  but  are  not  uncommon  before  the  age 
of  twenty  ;  they  occur  most  frequently  between  the  ages  of 
twenty  and  fifty,  and  seem  to  be  met  with  almost  in  equal 
numbers  between  the  three  periods  of  ten  years — from  twenty 
to  thirty,  from  thirty  to  forty,  and  from  forty  to  fifty. 

Sex. — Aneurisms  are  eight  times  more  frequent  in  males 
than  in  females.  Tumours  occur  almost  as  frequently  in 
females  as  in  males. 

Occupation. — Aneurism  is  much  more  common  amongst 
those  whose  occupations  necessitate  hard  manual  labour,  and 
in  soldiers,  sailors,  and  prostitutes.  Tumour  seems  also  more 
common  in  the  lower  orders,  but  it  is  not  more  frequent  in 
soldiers,  sailors,  prostitutes,  and  persons  who  follow  laborious 
occupations,  than  in  other  people. 

Hereditary  tendencies  and  temperament. — Aneurisms  occur 
most  frequently  in  persons  of  a  sanguine  temperament,  and 
in  those  families  in  which  diseases  of  the  heart  and  vascular 
system  are  hereditary.  Lympho-sarcomata  affect  persons  of 
a  lymphatic  and  scrofulous  habit.  A  hereditary  history  of 
cancer  cases  can  often  be  obtained  in  persons  suffering  from 
intra-thoracic  cancer. 

^■Etiology. — Strain,  syphilis,  alcoholic  excesses,  rheumatism, 


Diagnosis  of  Aneurism  of  the  l  horacic  Aorta.  731 

and  all  conditions  which  produce  arterial  degeneration  or 
increased  arterial  tension,  tend  to  produce  aneurism.  The 
causes  of  tumour  are  often  obscure.  In  some  cases  of  intra- 
thoracic cancer,  direct  injury  seems  to  have  been  the  exciting 
cause.  Lympho-sarcomata  seem  sometimes  to  be  due  to 
local  irritation.  In  one  of  my  own  cases  the  only  obvious  cause 
was  the  inhalation  of  gunpowder  smoke.  In  other  cases  the 
tumour  is  secondary  to  a  primary  cancer  or  sarcoma  in  some 
other  part  of  the  body.  The  intra-thoracic  tumours  which 
are  likely  to  be  mistaken  for  aortic  aneurisms  arc,  in  the  ma- 
jority of  cases,  primary,  and  originate  in  the  bronchial  glands 
or  the  remains  of  the  thymus.  Secondary  intra-thoracic 
tumours  usually  occur  as  nodules  (cancerous  infarctions  in 
many  cases)  in  the  pulmonary  tissue.  In  cases  of  this  de- 
scription the  symptoms  and  signs  of  thoracic  aneurism  are 
rarely  simulated. 

History  and  mode  of  development. — In  a  large  proportion, 
probably  in  at  least  50  per  cent,  of  the  cases  of  aneurism,  there 
is  a  history  of  syphilis.  In  cases  of  tumour  a  history  of  syphilis 
is  not  more  frequent  than  in  the  general  average  of  patients. 
In  aneurism  the  symptoms  may  develop  suddenly.  In  tumour 
the  symptoms  almost  always  develop  slowly  and  gradually. 

General  appearance. — Patients  suffering  from  aneurism 
often  present  all  the  external  appearances  of  perfect  health. 
The  subjects  of  intra-thoracic  cancer  or  lympho-sarcoma  are 
usually  pale,  emaciated,  and  cachectic  ;  it  is  quite  exceptional 
to  find  them  presenting  the  appearances  of  health.  (In  some 
cases  of  aneurism  the  expression  is  anxious,  the  patient  looks 
ill,  and  may  be  emaciated.  These  symptoms  are  seldom,  how- 
ever, striking,  unless  the  patient  is  exhausted  by  long-con- 
tinued pain  and  sleeplessness,  or  unless  the  aneurismal  tumour 
is  pressing  upon  the  oesophagus  or  thoracic  duct,  and  so  inter- 
fering with  nutrition.) 

Ttie  fottozving  pressure  symptoms  and  signs. — Lividity  ; 
oedema  of  the  face,  neck,  and  upper  extremities  ;  engorge- 
ment of  the  superficial  veins  of  the  head,  neck,  and  upper 
extremities — are  frequently  observed  in  both  cases  (aneurism 
and  tumour),  but  are  much  more  common  in  tumour. 


732  Diseases  of  the  Heart. 

Pain  is  very  much  more  prominent  in  aneurism  than  in 
tumour,  and  in  many  cases  is  one  of  the  most  important  points 
of  distinction  between  the  two  conditions.  The  pain,  which 
occurs  in  cases  of  tumour  is,  as  a  rule,  temporary,  and  is  often 
due  to  associated  pleurisy. 

Cough  seems  to  be  somewhat  more  frequent  in  tumour. 

Hemoptysis  is  much  more  frequent  in  tumour  than  in 
aneurism,  and  this  is  particularly  the  case  in  the  earlier  stages 
of  the  disease. 

Pressure  on  the  recurrent  laryngeal  nerve,  with  its  resulting 
symptoms,  is  more  frequent  in  tumour  than  in  aneurism,  if  we 
except  aneurisms  of  the  transverse  portion  of  the  aortic  arch, 
which  is  the  condition  above  all  others,  in  which  the  left  re- 
current laryngeal  nerve  is  implicated. 

Pressure  on  the  oesophagus,  with  resulting  dysphagia,  is 
more  frequently  the  result  of  tumour  than  of  aneurism.^ 

Differences  in  the  two  radial  pulses  are  more  frequentl}' 
observed  in  aneurism  than  in  tumour. 

Pressure  on  the  synipatJietic,  zvith  resulting  changes  in  the 
pupil  and  vascularity  on  one  side  of  the  head  and  neck,  seems 
to  be  more  frequent  in  aneurism,  but  is  often  observed  in 
tumour. 

Lateral  displacement  of  the  heart  is  much  more  common  in 
tumour. 

Physical  Signs  at  the  Seat  of  the  Tumour. — Inspection. — 
Prominence  of  the  chest  wall  is  very  much  more  common 
in  aneurism.  Aneurismal  prominence  is  usually  localised, 
with  a  broad  base  and  a  well-marked  apex,  whereas  a  pro- 
minence due  to  tumour  is  almost  always  a  general  bulging 
of  the  chest  wall.  Pulsation  over  the  prominence  is  rarely 
seen  in  the  case  of  tumour.  When  it  does  occur,  it  is  seldom 
localised,  but  is  usually  general,  the  whole  chest  wall  appear- 
ing to  be  raised  en  masse.  In  aneurism,  on  the  contrary, 
pulsation  is  common,  and  is  usually  localised  to  the  prominence 
itself     The  prominence  due  to  an  aneurism  is  more  frequently 

'  Most  of  these  statements  of  course  refer  to  aneurisms  and  tumours  as  a 
whole ;  no  attempt  has  been  made  to  compare  aneurisms  of  a  special  part  of  the 
aorta  with  tumours  of  a  special  part  of  the  thorax. 


Diagnosis  of  Aneiwism  of  the  Thoracic  Aoi'ta.  733 

situated  in  the  neighbourhood  of  the  second  right  interspace 
than  in  other  parts  of  the  thorax  ;  the  prominence  due  to  a 
tumour  rarely  occupies  this  position.  An  engorged  condition 
of  the  veins  of  the  thoracic  wall  is  more  frequently  seen  in 
tumour  than  in  aneurism.  CEdema  of  the  chest  wall  is  more 
common  in  tumour  than  in  aneurism.  (The  oedema  which  is 
due  to  aneurism  is  generally  hard,  and  associated  with  tender- 
ness on  pressure,  it  is  usually  in  fact,  inflammatory;  whereas, 
the  oedema  due  to  tumour  is  usually  soft  and  painless,  i.e. 
dropsical.)  Palpation.  —  Aneurismal  pulsation  is  frequently 
expansile,  and  often  equals  in  intensity  the  impulse  of  the 
heart.  The  pulsation  due  to  a  tumour  is  not  truly  expansile  ; 
it  is  usually  less  defined  than  the  pulsation  due  to  aneurism  ; 
it  seldom,  if  ever,  equals  in  intensity  the  cardiac  impulse,  but  is 
usually  feeble  and  diffused  over  an  extensive  area  of  the  chest 
wall.  The  vocal  fremitus  is  often  present  over  the  dull  area 
of  a  tumour,  but  is  absent  over  the  dull  area  of  an  aneurism. 
Percussion. — The  dulness  due  to  aneurism  is  generally  more 
localised,  and  more  closely  related  to  the  course  of  the  aorta 
than  the  dulness  due  to  tumour.  This  point  is  one  of  great 
practical  importance.  Auscultation  often  gives  very  valuable 
information.  In  cases  of  tumour  the  breath-sounds  can 
generally  be  heard  over  the  position  of  the  dulness,  usually 
in  the  form  of  bronchial  or  tubular  breathing,  and  the  vocal 
resonance  is  usually  present  and  often  increased.  In  cases  of 
aneurism,  the  breath-sounds  and  vocal  resonance  are  not,  as  a 
rule,  audible  over  the  area  of  dulness.  An  exception  to  this 
statement  occurs  in  those  rare  cases  of  thoracic  aneurism  in 
which  the  aneurismal  sac  is  filled  with  laminated  fibrine,  and 
is  in  close  contact  with  the  trachea  or  large  bronchi.  The 
following  is  a  case  in  point : — 

Case  of  Aneurism  of  the  Aorta,  Innominate,  Left  Common  Carotid,  Right 
Common  Carotid,  and  Left  Subclavian,  Arteries,  simulating  Solid 
Intra-thoracic  Tumour. 

M.  F.,  cet.  64,  a  striker,  was  admitted  to  the  Newcastle-on-Tyne  In- 
firmary under  my  care  on  i8th  February  1878,  suffering  from  oedema  of 
the  face,  neck,  and  upper  extremities,  and  complaining  of  shortness  of 
breath  on  the  least  exertion. 


734  Diseases  of  the  Heart. 

Previous  History. — The  patient,  who  had  been  under  treatment  for 
some  days  as  an  out-patient,  stated  that  he  had  been  through  hfe  an  un- 
usually strong  healthy  man.  He  had  neither  suffered  from  rheumatism 
nor  syphilis.  His  present  illness  commenced  some  six  weeks  previous  to 
admission,  with  shortness  of  breath  on  e.xertion.  This  was  followed  by 
swelling  of  the  face  and  hands.  He  had  of  late  occasionally  experienced 
a  slight  pain  under  the  manubrium  sterni  and  in  each  shoulder.  He  had 
lost  flesh,  his  voice  had  become  'thicker'  than  it  used  to  be,  and  there 
liad  been  some  dysphagia. 

Condition  on  Admission.— The  patient  was  extremely  dirty,  the  skin 
being  of  a  deep  brown  colour  ;  this  was  so  marked  that  the  case  was  sent 
to  me  as  one  of  Addison's  disease.  The  nipples,  genitals,  and  axillae, 
were  not  specially  pigmented.  The  patient  was  fairly  nourished,  though 
he  stated  that  he  had  lost  flesh.  The  base  of  the  neck  was  ver)^  much 
swollen  and  hard.  The  face,  upper  extremities,  and  upper  part  of  the 
thoracic  wall  were  oedematous.  The  superficial  veins  of  the  thorax  and 
abdomen  were  engorged  and  prominent.  (The  veins  of  the  head,  neck, 
and  upper  extremeties  were  also  engorged,  but  were  in  great  part  hidden 
by  the  oedema.)     There  was  well-marked  prascordial  vascularity. 

The  lips  were  swollen  and  blue. 

The  slightest  exertion,  such  as  getting  out  of  bed  to  urinate,  caused 
great  shortness  of  breath.  When  at  rest  the  breathing  was  natural. 
Fopd  seemed  to  stick  at  a  point  corresponding  to  the  manubrium  sterni. 
There  was  some  cough  and  frothy  expectoration.  The  pupils  were  equal 
and  contracted.  The  larjnx  was  not  examined.  The  radial  pulses  were 
equal  both  in  time  and  volume.  The  carotid  pulses  seemed  equal,  but 
the  pulsation  in  these  vessels  was  difficult  to  feel  owing  to  the  brawny 
cedema  of  the  neck. 

The  heart  was  of  natural  size  ;  its  valves  healthy  ;  its  action  weak. 

There  was  well-marked  percussion  dulness  over  the  manubrium 
sterni,  and  on  each  side  of  it  especially  to  the  left.  On  auscultation, 
tubular  breathing  and  greatly  increased  vocal  resonance  were  heard 
under  the  right  sterno-clavicular  articulation.  Over  the  manubrium 
the  breath-sounds  were  indistinct.  The  heart  sounds  were  ver>'  faintly 
and  distantly  heard  over  the  same  part.  Under  the  left  sterno-clavicular 
articulation,  and  to  the  left  of  it,  the  breathing  was  bronchial.  Poste- 
riorly, the  respirator}^  murmur  was  weaker  in  the  right  than  in  the  left 
lung.  Bronchial  rales  were  heard  here  and  there  over,  the  chest.  There 
was  no  glandular  enlargement.  The  blood  was  normal,  except  that  the 
adhesiveness  of  the  red  globules  was  increased. 

Diagnosis. — The  diagnosis  was  an  intra-thoracic  tumour.  It  was 
thought  to  be  solid  because  of: — 

\st.  The  marked  venous  engorgement  and  local  oedema. 

id.  The  absence  of  any  decided  pain. 

2,d.  The  somewhat  extensive  character  of  the  dulness. 


Diagnosis  of  Anciirism  of  tJic  Thoracic  Aorta.     735 

4M.  The  tubular  breathing  and  increased  vocal  resonance  under  the 
right  clavicle. 

^ih.  The  absence  of  any  marked  vascular  sounds  over  the  dull  area. 

bth.  The  non-accentuation  of  the  aortic  second  sound  at  the  base  of 
the  heart. 

The  treatment  consisted  in  rest  in  bed  and  the  administration  of  full 
doses  of  iodide  of  potassium. 

Progress  of  t]ie  Case. — On  27th  February  the  patient  was  decidedly 
better,  the  oedema  was  disappearing. 

On  6th  March,  the  cedema  having  almost  gone,  the  thorax  was  again 
carefully  examined,  and  important  alterations  were  observed.  The  heart's 
action  was  considerably  stronger  than  before.  Well-marked  pulsation 
could  be  felt  in  the  supra-sternal  notch  over  the  manubrium  sterni,  the 
heart  sounds  could  be  distinctly  heard,  and  they  presented  that  toneless 
superficial  character  which  is  rightly  considered  as  characteristic  of  an 
aneurism.  The  radial  pulses  were  equal  both  in  time  and  volume  ;  a 
sphygmographic  tracing  showed  nothing  of  importance,  the  only  dif- 
ference being  that  the  percussion  stroke  was  slightly  shorter  in  the  right 
than  in  the  left.  (See  figs.  295  and  296.)  (This  is  a  point  of  some  import- 
ance, for  a  good-sized  aneurism  of  the  innominate  was  found  after  death. 
The  case  does  not,  however,  disprove  Dr  Mahomed's  observations  as 
to  the  diagnosis  of  innominate  aneurism  by  means  of  the  sphygmograph, 
for  the  sac  of  the  aneurism  was  so  filled  with  coagulum  that  the  normal 
diameter  of  the  blood  channel  was  accurately  preserved.) 


Fig.  295. — (Right  radial.)  Pressure  t^oz.     Fig.  296. — (Left  radial).   Pressure  t^  oz. 

Fig.  295  and  296. — Case  of  Multiple-Aneurisms. — M.F.,  set.  64,  admitted  to  the 
Newcastle  Infirmary  i8th  February  1878,  suffering  from  symptoms  of  intra- 
thoracic pressure.  Died  loth  March.  Post-mortem  showed  dilatation  and 
small  aneurism  of  aortic  arch.  Fusiform  aneurisms  of  the  innominate,  left 
common  carotid  and  left  subclavian  arteries,  just  above  their  origins.  The 
aneurisms  were  filled  with  firm  clots,  through  which  a  straight  narrow 
channel  for  the  blood  remained. 
On  Sth  March  the  patient  was  worse  ;  the  cedema  had  returned.     At 

the  time  of  my  visit  he  was  seized  with  a  severe  rigor,  during  which  the 

temperature  rose  to  io5"'2  Fahr. 

On  gth  March  he  spat  up  some  muco-  purulent  matter  mixed  with 

blood.     The  base  of  the  neck  was  very  hard  and  brawny,  and  the  skin 

had  a  red,  erythematous  appearance. 


736  Diseases  of  the  Heai't. 

On  loth  March  he  died. 

"^'Sx^ post-mortem  was  made  twenty-seven  hours  after  death.  The  base 
of  the  neck  was  much  swollen  and  infiltrated  with  serum  containing 
leucocytes. 

The  aorta,  from  its  origin  to  the  termination  of  the  transverse  portion 
of  the  aortic  arch,  was  veiy  much  dilated  and  atheromatous.  (Specimen 
exhibited  at  May  meeting  of  the  Edinburgh  Medico-Chirurgical  Society.) 
A  sacculated  aneurism,  the  size  of  a  small  cherry,  projected  from  the 
anterior  surface  of  the  aortic  arch.  This  small  aneurism,  to  the  outer 
surface  of  which  the  lung  was  firmly  adherent,  was  completely  filled  with 
firm  decolorised  clot. 

The  innominate  artery  was  irregularly  dilated  to  the  size  of  a  ban- 
tam's egg.  The  vessel,  at  its  origin  and  at  its  termination  was  of  normal 
calibre.  The  sac  of  the  aneurism  pressed  upon  and  was  adherent  to  the 
trachea.  The  left  common  carotid  artery,  immediately  after  rising  from 
the  aortic  arch,  was  uniformly  dilated  to  the  size  of  a  damson.  The 
right  common  carotid,  immediately  after  its  origin  from  the  innominate, 
was  dilated  to  the  size  of  a  small  cherry.  The  left  subclavian,  imme- 
diately above  its  origin  from  the  aorta,  was  slightly  dilated. 

Firm  coagula  channelled  in  their  centres  filled  the  aneurisms  of  the 
innominate,  left  common  carotid,  right  common  carotid,  and  left  sub- 
clavian arteries.  (See  figs.  293  and  294.)  The  channels  in  the  coagula 
exactly  corresponded  in  their  calibre  to  the  normal  size  of  these  vessels. 

The  superior  vena  cava  was  pressed  upon  and  greatly  obstructed  by 
the  dilated  arch.  The  heart  was  normal,  its  weight  10  oz.  The  other 
arteries  throughout  the  body  were  natural.  Both  lungs  were  adherent 
at  their  apices.  The  upper  lobe  of  the  left  lung  was  in  places  consoli- 
dated owing  to  the  deposit  of  small  masses  of  black  pigment.  The 
trachea  and  bronchi  were  inflamed.     The  other  organs  were  normal. 

The  cause  of  the  aneurismal  dilatation  of  the  arch  and  its  branches 
was  not  ascertained. 

The  character  of  the  heart  and  aortic  sounds  over  the  dull 
area  of  a  tumour  varies  in  different  cases.  In  some,  the  car- 
diac or  aortic  sounds  are  inaudible  ;  more  frequently,  both 
cardiac  sounds  are  heard,  free  from  murmur  and  weaker  and 
more  distant  than  over  the  heart  itself ;  in  a  third  group  of 
cases  a  systolic  murmur  is  audible,  it  is  sometimes  followed 
by  a  second  sound,  which  is  not,  however,  accentuated.  In 
many  cases  the  second  sound  is  faint  or  absent.  The  auscul- 
tatory phenomena  which  are  heard  over  an  aneurismal  sac 
have  been  fully  detailed,  and  need  not  again  be  described. 
Let   me  repeat,  however,  that  a   murmur  is  more  frequently 


Diagnosis  of  Thoracic  Aneu7^isin.  737 

absent  than  present  in  those  cases  in  which  the  cardiac  valves 
are  healthy  ;^  and  that  an  accentuated  aortic  second  sound, 
with  or  without  a  systolic  murmur,  is  of  great  diagnostic  value, 
when  other  symptoms  and  signs  of  aneurism  are  present. 

Associated  diseased  conditions.  —  Cardiac  valvular  lesions 
(more  especially  aortic  regurgitation)  and  general  atheroma 
are  frequently  present  in  aneurism,  but  comparatively  rare  in 
tumour.  Pulmonary  lesions,  pleurisy,  glandular  enlargements, 
and  new  growths  in  the  liver  and  other  internal  organs  are 
often  associated  with  intra-thoracic  (cancerous  and  sarcoma- 
tous) tumours.  The  associated  diseased  conditions  and  the 
general  pathological  tendencies  of  the  individual  are  therefore 
of  the  greatest  importance  from  a  diagnostic  point  of  view. 

The  progress  of  the  case  and  the  results  of  treatment. — 
Intra-thoracic  tumours  (cancerous  and  sarcomatous  growths) 
steadily,  and,  as  a  rule,  rapidly  progress  from  bad  to  worse,  and 
are  not  amenable  to  treatment,  though  Walshe  has  seen  tem- 
porary improvement  in  some  cases  of  cancer.^  The  progress 
of  aneurism  is,  as  a  rule,  much  more  gradual,  and  the  symp- 
toms can,  in  most  cases,  be  temporarily  relieved  by  treatment 
(rest,  dieting,  and  iodide  of  potassium). 

Step  No.  2.  If  an  aneurism  is  present,  is  it  an  a)ieurism 
of  the  thoracic  aorta  ? 

Aneurisms  of  the  transverse  portion  of  the  aortic  arch  are, 
in  many  cases,  with  difficulty  distinguished  from  ancnrisms  of 
the  innominate  artery.  The  distinction  is  a  matter  of  prac- 
tical importance,  for  surgical  treatment,  which  is  justifiable 
and  advisable  in  many  cases  of  innominate  aneurism,  is  hardly 
to  be  recommended  when  the  aneurism  is  aortic.  In  many 
cases  the  aneurismal  tumour  involves  the  transverse  portion 
of  the  aortic  arch  and  the  innominate  artery  ;  and  it  is  more 

'  In  speaking  of  the  value  of  a  sysotlic  murmur  in  cases  of  this  description 
Stokes  says  : — '  If  we  suppose  a  case  in  which  the  evidences  on  both  sides  were 
nearly  balanced,  the  existence  of  a  single  soft  systolic  bellows  murmur  should 
incline  our  opinion  towards  cancer.  Bellows  murmur  in  aneurism  of  the  arch  is  a 
more  rare  circumstance  than  has  been  supposed.' — Diseases  of  the  Heart  and 
Aorta,  p.  605. 

"  Diseases  of  the  Heart,  p.  579- 

AAA 


738  Diseases  of  the  Heart. 

especially  in  those  cases  in  which  the  symptoms  and  signs  of 
innominate  aneurism  are  present,  and  in  which  the  question 
of  operative  procedure  therefore  arises,  that  it  is  important 
to  determine  whether  the  aneurismal  tumour  involves  the 
aortic  arch  or  not.  In  many  cases  the  decision  is  easy,  in 
others  difficult,  in  some  cases  impossible. 

The  question  is  to  be  decided  chiefly  by  careful  percussion 
of  the  aortic  arch.  Attention  must  also  be  directed  to  the 
following  points : — 

1.  The  position  of  the  aneurism. — Innominate  aneurisms 
are  usually  situated  to  the  right  of  the  middle  line,  and  ex- 
tend chiefly  upwards  into  the  neck.  The  innominate  artery- 
rises,  it  will  be  remembered,  on  the  level  of  the  upper  edge 
of  the  first  interspace,  or  that  of  the  lower  part  of  the  first 
cartilage,  behind  the  right  half  of  the  upper  sternal  region, 
passes  upwards  and  to  the  right,  bifurcating  to  the  right  of 
the  trachea,  or  a  little  above  and  to  the  right  of  the  sterno- 
clavicular joint.^  When,  therefore,  the  aneurismal  tumour  is 
situated  under  the  right  sterno-clavicular  articulation,  and 
when  percussion  fails  to  demonstrate  any  distinct  enlargement 
of  the  aortic  arch,  the  aneurism  is  probably  innominate. 

2.  The  effects  of  pressiwe  on  the  right  coinino)i  carotid  and 
right  subclavian  arteries. — Firm  pressure  on  the  vessels  arising 
from  the  innominate  trunk  arrests,  it  is  said,  or  materially 
lessens  the  pulsation  of  an  innominate  aneurism,  but  fails  to 
produce  any  material  effect  upon  aneurisms  of  the  aortic  arch. 
This  and  the  following  points  are,  however,  of  little  value  in 
deciding  whether,  in  cases  of  innominate  aneurism,  the  sac 
involves  the  arch  of  the  aorta  or  not. 

3.  The  condition  of  the  pulse. — Aneurisms  of  the  innominate 
are  much  more  likely  to  modify  the  characters  of  the  right 
radial  pulse  (in  the  manner  described  on  p.  283)  than  aneurisms 
of  the  aortic  arch. 

4.  The  lurture  of  the  pressure  symptoms. — Aneurisms  of  the 
innominate,  which  rarely  extend  to  the  right  of  the  middle 
line,  are  much  less  likely  to  produce  pressure  upon  the  trachea, 
oesophagus,  and  left  recurrent  laryngeal  nerve  but  are  more 

'  Walshe,  Diseases  of  the  Hca)-t,  p.  6, 


Pt'-o^nosis  of  Aneurism  of  the  TJioracic  Aorta.     739 

likely  to  press  upon  the  strands  of  the  right  brachial  plexus, 
and  upon  the  right  recurrent  laryngeal  nerve,  than  aneurisms 
of  the  aortic  arch. 


Prognosis. — Aneurisms  of  the  thoracic  aorta  almost  in- 
variably prove  fatal,  the  few  cures  which  have  been  met  with, 
being  amongst  the  curiosities  of  medicine  ;  the  prognosis,  as 
regards  the  ultimate  result,  is,  therefore,  most  unfavourable. 
The  duration  is  a  matter  of  the  greatest  uncertainty,  for  there 
is  always  a  risk  of  rupture  and  of  sudden  death.  Our  opinion, 
as  to  the  probable  duration  of  the  case,  must  be  guided  to  some 
extent  by  {a)  the  stage  of  the  disease,  {p)  the  position  of  the 
aneurism,  and  {c)  the  circumstances,  surroundings,  and  mental 
temperament  of  the  patient.  The  larger  the  sac,  other  things 
being  equal,  the  shorter  the  probable  duration  of  the  case. 
Aneurisms  of  the  sinuses  of  Valsalva  probably  kill  sooner 
than  aneurisms  of  any  other  part  of  the  aorta.  Aneurisms  of 
the  ascending  portion  of  the  arch,  above  the  sinuses  of  Val- 
salva, which  make  their  v/ay  forwards,  have,  on  the  average, 
the  longest  duration.  Aneurisms  of  the  transverse  and  de- 
scending portions  of  the  aortic  arch,  and  of  the  descending 
thoracic  aorta,  probably  occupy  (as  regards  duration)  a  mid- 
position,  i.e.  they  usually  last  longer  than  aneurisms  of  the 
sinuses  of  Valsalva,  but  shorter  than  aneurisms  of  the  ascend- 
ing portion  of  the  arch. 

When  the  sac  is  pressing  upon  the  trachea,  upon  a  main 
bronchus,  or  upon  the  oesophagus,  the  fatal  termination  is,  as 
a  rule,  close  at  hand. 

Patients  who  are  obliged  to  exert  themselves  in  order 
to  gain  a  livelihood,  more  particularly  those  who  have  to 
follow  laborious  occupations,  are  at  a  serious  disadvantage, 
for  rest  and  the  avoidance  of  all  strain  are  the  most  import- 
ant means  of  treatment.  Persons  of  an  irritable  disposition, 
those  who  are  easily  excited,  who  will  not  submit  to  the 
restraints  of  treatment,  and  those  who  indulge  in  alcoholic 
excesses,  are  also  heavily  handicapped  ;  in  them  the  average 
duration  of  the  disease  is  considerably  shorter  than  in  other 
people. 


740  Diseases  of  the  Heart. 

The  associated  pathological  conditions  must  also,  of  course, 
be  taken  into  account  in  forming  an  opinion  as  to  the  probable 
duration  of  the  case. 

Treatment. — The  great  object  of  treatment  in  the  case  of 
all  aneurisms  is  to  endeavour  to  effect  a  cure  by  causing 
solidification  or  contraction  of  the  sac. 

In  the  case  of  aneurisms  of  the  thoracic  aorta,  surgical 
means  of  cure  are,  with  the  exception  of  galvano-puncture, 
which  will  be  presently  considered  in  detail,  inadmissible. 
Reliance  must,  therefore,  be  chiefly  placed  upon  general 
measures  and  the  use  of  drugs. 

The ^;'.y/ indication  is  to  keep  the  circulation  as  tranquil 
as  possible.  In  carrying  out  this  indication,  the  intelligent 
co-operation  of  the  patient  is  essential.  It  is  necessary, 
therefore,  to  explain  to  him  the  nature  of  the  disease,  the 
things  which  are  to  be  avoided,  and  the  exact  objects  which 
we  have  in  view. 

In  the  first  place,  all  bodily  exertion  and  mental  excite- 
ment, which  increase  the  intra-arterial  blood  pressure,  are  to 
be  avoided.  The  ideal  treatment  is  to  keep  the  patient  at 
absolute  rest  in  bed  ;  but  since  this  treatment  to  be  at  all 
effectual  must  be  of  long  duration,  patients  will  not,  or 
cannot,  with  rare  exceptions,  submit  to  it.  Absolute  rest  in 
bed  undoubtedly  gives  the  patient  the  best  chance,  but  it  is 
doubtful  if  many  actual  cures  would  be  effected  even  if  this 
indication  could  always  be  strictly  carried  out.  Whenever 
the  mental  temperament  and  circumstances  of  the  patient 
will  permit,  the  ideal  treatment  should  be  enforced.  When 
the  patient  will  not  or  cannot  lie  in  bed,  the  amount  of 
muscular  action  should  be  as  small  as  possible,  in  particular, 
sudden  efforts  or  strains  are  to  be  avoided. 

In  the  second  place,  all  causes  of  mental  excitement,  espe- 
cially of  sudden  mental  excitement,  are  to  be  guarded  against. 

In  the  third  place,  the  diet  must  be  strictly  regulated.  The 
amount  of  food  allowed  should  be  as  small  as  is  compatible 
with  the  proper  nutrition  of  the  body  and  the  maintenance  of 
the  coagulating  properties  of  the  blood  ;    it  must   be  easily 


Treatment  of  Aneurism  of  the  Thoracic  Aorta.     741 

digested,  but  at  the  same  time  nutritious.  The  amount  of 
liquid  must  also  be  restricted,  and  alcoholic  stimulants  abso- 
lutely forbidden.  Mr  Tufnell,  whose  treatment  of  thoracic 
aneurisms  by  rest  and  low  diet  has  been  so  successful,  limits 
the  amount  of  food  to  : — -2  oz.  of  bread  and  butter  and  2  oz.  of 
new  milk  for  breakfast ;  2  or  3  oz.  of  bread,  and  2  or  3  oz.  of 
meat  for  dinner,  with  2  to  4  oz.  of  milk  or  claret ;  2  oz.  of 
bread  and  2  oz.  of  milk  for  supper.  Personally  I  have  never 
enforced  such  a  very  restricted  diet.  I  always,  however,  impress 
the  patient  with  the  importance  of  strict  moderation  both  as 
regards  food  and  drink. 

In  WxQ  fourth  place,  the  condition  of  the  bowels  must  be 
carefully  regulated,  so  that  all  straining  at  stool  is  avoided. 
Sexual  intercourse  must  of  course  be  forbidden. 

In  the  fifth  place,  drugs  which  reduce  the  arterial  tension, 
and  which  experience  has  found  useful,  are  to  be  given. 
Iodide  of  potassium,  is  by  far  the  most  valuable  remedy. 
When  the  case  first  comes  under  observation,  and  more  espe- 
cially when  pain  is  a  prominent  symptom,  the  drug  should 
be  given  in  full  doses  (30  grs.  three  times  a  day)  ;  as  soon  as 
the  pain  subsides  the  dose  may  be  reduced,  though  personally 
I  have  been  in  the  habit  of  continuing  the  full  dose  so  long  as 
it  is  satisfactorily  borne.  Dr  George  Balfour,  who  has  done 
so  much  to  establish  the  iodide  plan  of  treatment  in  this 
country,  thinks  that  the  large  doses  which  he  formerly  recom- 
mended are  unnecessary  ;  he  now  gives  smaller  doses.  The 
proper  dose  for  each  case  is,  he  states,  that  which  will  lower 
the  blood  pressure  without  increasing  the  frequency  of  the 
cardiac  contractions.  In  speaking  of  the  manner  in  which  the 
dose  which  is  suitable  for  each  case  is  to  be  ascertained,  he 
states  : — '  Accordingly,  those  eases  which  came  next  under 
treatment  were  put  to  bed  for  a  few  days  without  further 
treatment,  their  pulse-rate  being  carefully  taken  night  and 
morning.  So  soon  as  the  average  pulse-rate  in  recumbency 
had  been  sufficiently  ascertained,  10  grs.  of  iodide  of  potas- 
sium in  some  bitter  infusion,  usually  chiretta,  were  given 
three  times  a  day.  If  the  pulse-rate  remained  unchanged, 
the  dose  was  increased  to    15  grs.  three  times  a  day,  and 


742  Diseases  of  tJic  Heart. 

we  have  not  yet  been  able  to  get  beyond  this  dose  ;  while 
very  often  we  have  not  been  able  to  give  more  than  lO  grs. 
without  raising  the  pulse-rate.'^ 

The  exact  method  in  which  the  iodide  of  potassium  acts  is 
doubtful.  Some  authorities  think  that  it  produces  some  modi- 
fication in  the  blood,  which  favours  coagulation  and  clotting 
within  the  sac.  Dr  Balfour  thinks  that  it  acts  '  mainly  by 
some  peculiar  action  on  the  fibrous  tissue,  whereby  the  walls 
of  the  sac  are  thickened  and  contracted,  while  if  coagulation 
should  take  place  within  the  sac,  it  plays  but  a  very  secondary 
and  unimportant  part,  depends  for  its  occurrence  solely  on  the 
remora  of  the  blood,  and  is  in  no  respect  due  to  the  iodide  of 
potassium.'-  He  states  that  'hypertrophy  of  the  muscular  coat, 
where  that  still  exists,  and  of  the  adventitia,  with  concomitant 
contraction,  are  found  in  all  aneurisms  which  have  been  treated 
with  the  iodide  with  any  measure  of  success.'^  My  own  observa- 
tions lead  me  to  doubt  the  occurrence  of  hypertrophy  of  the  mus- 
cular coat  in  the  wall  of  the  sac.  I  believe  that  the  iodide  acts 
chiefly  by  reducing  the  blood  pressure  and  relieving  the  tension 
within  the  sac — a  point  which  Dr  Balfour  also  thinks  is  of  the 
greatest  importance — and  partly,  perhaps,  by  removing  the 
endarteritis  obliterans,  which  is  often  present,  more  especially 
in  syphilitic,  cases,  in  the  minute  arteries  which  ramify  in  the 
walls  of  the  sac  and  which  supply  it  with  nutrient  fluid.  The 
administration  of  small  doses  of  chloral  (/  grains  three  times 
a  day)  has  appeared  to  me  beneficial  in  some  cases  in  which 
the  arterial  tension  is  distinctly  increased.  Possibly  nitro- 
glycerine might  be  advantageous  in  cases  of  this  description. 
The  external  application  of  cold  is  the  best  means  of  relieving 
temporary  overaction  of  the  heart.  Aconite  is  also  recom- 
mended by  some  writers.  Both  means  are  at  the  best,  pallia- 
tives, and  produce  no  permanent  benefit.  In  those  cases  in 
which  there  is  a  tendency  to  cardiac  excitement,  our  main 
object  should  be  to  ascertain  the  cause  of  the  over  action 
and  to  remove  it ;  and  in  this  connection  it  is  important  to 
remember  that  starvation  or  anything  else  which  causes 
anaemia,  produces  an  irritable  condition  of  the  heart,  in  which 

'  Diseases  of  the  Heart,  p.  458.       -  Ibid.,  second  edition,  p.  454.       ^  Ibid.  p.  457. 


Treatment  of  TJioracic  Aneiirisius.  743 

palpitation  is  readily  excited  by  mental  agitation  or  slight 
bodily  exertion.  Care  .must,  therefore,  be  taken  that  while 
the  diet  is  restricted,  it  is  not  reduced  to  such  a  point  as  will 
produce  anjemia  and  cardiac  irritability. 

The  hypodermic  injection  of  ergotine  was  recommended 
by  Langenbeck  some  years  ago  as  a  means  of  producing  con- 
traction of  the  sac  ;  but  subsequent  observers  have  not  met 
with  the  same  favourable  results  which  he  described. 

It  has  been  proposed  to  produce  coagulation  within  the 
sac  by  mechanical  means,  such  as  ligature  of  the  great  vessels 
arising  from  the  aortic  arch,  the  introduction  of  iron  wire 
or  horse  hair,  or  the  injection  of  perchloride  of  iron  into  the 
sac,  and  by  galvano-puncture.  The  results  of  ligaturing  the 
vessels  arising  from  the  sac  are  not  favourable.  Surgical 
interference  of  this  sort  is,  in  my  opinion,  seldom  justifiable, 
and  so  far  as  I  can  form  a  judgment,  inferior  to  galvano- 
puncture.  The  introduction  of  iron  wire  or  horse  hair  into 
the  sac,  and  the  injection  of  perchloride  of  iron  or  other 
astringents  should  never  be  attempted. 

Galvajio-puncture. — This  method  of  treatment  should  only 
be  attempted  when,  after  a  fair  and  prolonged  trial,  the 
treatment  by  iodide  of  potassium,  rest,  and  dieting,  has  failed, 
or,  in  those  cases  in  which  the  sac  is  obviously  on  the  point 
of  rupturing,  and  in  which  it  is,  therefore,  necessary  to  have 
recourse  to  some  plan  of  treatment  calculated  to  produce 
immediate  relief.  Galvano-puncture  may  be  performed  with 
two  distinct  objects,  viz. : — 

(i)  To  coagulate  the  whole  contents  of  the  sac  at  one 
sitting. 

(2)  To  form  a  small,  firm  clot,  which  will  act  as  a  nucleus 
on  which  layers  of  coagula  will  be  subsequently  deposited. 

For  the  successful  performance  of  galvano-puncture  it  is 
necessary  to  use  a  current  of  considerable  strength.  Some 
writers  recommend  the  Leclanche  element,  which  is  so  con- 
venient for  many  purposes,  but  the  Stohrer's  element  is 
probably,  as  Dr  de  Watteville  points  out,  better  suited  for 
electrolysis.^     The  needles  must  be  well  insulated,  and  there 

'  liledical  Electricity,  second  edition,  pp.  67  and  200. 
i 


744  Diseases  of  the  Heart. 

must  be  no  shoulder  where  the  insulating  material  joins  the 
barb.  Authorities  differ  as  to  whether  one  or  both  needles 
should  be  introduced  into  the  sac.  It  is  probably  unnecessary 
to  introduce  a  needle  connected  with  the  negative  pole  into 
the  sac  ;  one  or  more  needles  should,  therefore,  be  introduced 
and  connected  with  the  positive  pole,  and  the  negative  pole 
connected  with  a  large  flat  copper  electrode  (covered  with 
wash-leather)  placed  on  the  abdomen.  Dr  de  Wattevillc 
states  that  '  in  order  to  avoid  the  burning  sensation  and 
vesication  of  the  skin,  a  layer  of  modeller's  clay  may  be 
effectually  placed  between  the  plate  and  skin,  as  suggested 
by  Dr  Apostoli  of  Paris.'-  Before  the  needle  or  needles  are 
introduced  into  the  sac,  the  physician  must  see  that  the 
battery  is  in  working  order  ;  this  is  best  tested  by  observing 
the  coagulating  power  of  the  current  on  albumen.  (The  white 
of  an  (t^ig  is  to  be  placed  in  a  saucer,  and  the  needles,  con- 
nected with  the  battery,  inserted  in  it.  On  the  passage  of 
the  current  a  small  firm  clot  is  produced  at  the  positive,  and 
a  large,  loose,  whipped-up,  frothy  clot,  around  the  negative 
needle.)  The  exact  nature  of  the  procedure  must  be  explained 
to  the  patient,  and  he  must  be  cautioned  not  to  make  any 
sudden  movement  when  the  needle  is  being  introduced.  The 
sensibility  of  the  skin  may  be  deadened  at  the  seat  of  the 
proposed  puncture,  by  the  application  of  ice  or  ether  spray, 
but  it  is  not  desirable  to  freeze  the  skin  thoroughly,  lest 
its  vitality  should  be  impaired  and  the  rupture  of  the  sac 
hastened.  The  needles,  which  should  be  very  sharp,  must  be 
slowly  but  steadily  introduced  into  the  sac.  After  the  opera- 
tor is  satisfied  that  the  insulating  material  is  well  through  the 
wall  of  the  sac,  the  needle  may  be  connected  with  the  battery. 
The  duration  of  the  seance  varies  with  the  object  of  treat- 
ment. When  it  is  desired  to  coagulate  the  whole  contents  of 
the  sac,  the  operation  must  be  continued  until  the  sac  is  felt 
to  be  firm  and  solid.  Two  or  three  hours  may  be  required  for 
this  purpose.  When,  on  the  other  hand,  the  object  is  to  pro- 
duce a  small,  firm  coagulum,  the  current  should  not  be 
passed  through  the  sac  for  more  than  twenty  minutes  or  half 
'  Medical  Electricity,  second  edition,  p.  199. 


Treatment  of  Aneurism  of  the  Thoracic  Aorta.    745 

an  hour.  Should  bleeding,  or  any  other  untoward  symptom 
occur  during  the  course  of  the  operation,  the  current  should 
be  at  once  '  broken  '  and  the  needles  withdrawn.  The  needles 
are  best  withdrawn  by  means  of  a  slow  rotatory  movement. 
A  pad  of  lint  must  then  be  applied  over  the  point  of  puncture. 

It  is  usually  necessary  to  repeat  the  galvano-puncture 
more  than  once.  Between  the  seances  the  treatment  by  rest, 
iodide  of  potassium,  and  restricted  diet,  must  be  steadily  per- 
severed with.  The  operation  is  apt  to  be  followed  by  inflam- 
mation of  the  sac  wall.  This  is  the  great  danger.  The  risks 
of  bleeding  (either  during  the  operation  or  after  the  withdrawal 
of  the  needles)  and  of  embolism  are  extremely  slight. 

Galvano-puncture  is,  I  repeat,  chiefly  useful  as  a  last  re- 
source. It  should  only  be  attempted  in  those  cases  in  which 
(i)  a  prolonged  and  patient  trial  has  been  given  to  rest,  diet, 
and  iodide  of  potassium,  and  in  which  that  method  has 
failed  ;  or  (2)  in  those  cases  in  which  the  aneurism  is  pro- 
gressing rapidly  or  is  on  the  point  of  rupturing,  and  in  which, 
therefore,  it  is  necessary  at  all  hazards  to  arrest  the  progress 
of  the  disease  without  delay.  The  treatment  is  most  likely  to 
be  beneficial  in  those  cases  in  which  the  aneurism  is  distinctly 
sacculated,  and  more  especially  when  the  chest  wall  has  be- 
come perforated,  and  an  external  false  aneurism  has  been 
formed.  Galvano-puncture  is  not  advisable  in  those  cases  in 
which  aneurismal  dilatation  is  general,  globular,  or  fusiform. 

For  the  relief  of  urgent  symptoms  other  measures  may  of 
course  be  employed. 

Pain,  which  is  such  a  prominent  symptom  in  many  cases 
of  aortic  aneurism,  is  best  relieved  by  the  administration  of 
large  doses  of  iodide  of  potassium.  In  some  cases,  it  is  neces- 
sary to  give  hypodermic  injections  of  morphia,  but  the  system^ 
atic  administration  of  this  drug  is  seldom  required  except 
during  the  first  few  days  of  treatment,  i.e.  when  the  patient 
first  comes  under  observation,  and  before  the  iodide  has  had 
time  to  act. 

Dyspna:a,  dysphagia,  Juenioptysis,  and  other  prominent 
symptoms,  must  be  met  by  appropriate  remedies.  I  need  not 
go    into    details,   further  than   to   say,   that   attention   to   the 


746  Diseases  of  the  Heai't. 

mechanical  position  of  the  parts  and  the  administration  of 
such  remedies  as  iodide  of  potassium,  the  external  application 
of  cold  to  the  surface  of  the  tumour,  and  subcutaneous  injec- 
tions of  ergotine,  are  the  most  likely  means  of  giving  relief 
When  the  dyspnoea  is  very  severe,  and  clearly  lar}'ngcal  in 
cliaractcr,  the  question  of  tracheotomy  has  to  be  considered. 
The  operation  should  only  be  performed  when  the  observer 
is  satisfied  that  the  dyspnoea  is  due  to  laryngeal  paralysis  or 
spasm.  It  is  of  course  quite  useless  and  inadmissible  in  those 
cases  in  which  the  dyspnoea  is  due  to  compression  of  the 
trachea  or  bronchi.  Bristowe's  opinion — -that  the  paroxysmal 
attacks  of  dyspnoea,  which  many  observers  ascribe  to  spasms 
or  paralysis  of  the  glottis,  in  reality  depend  upon  the  pressure 
of  the  sac  on  the  trachea — must  be  remembered. 

When  the  sac  threatens  to  rupture  externally,  galvano- 
puncture  is,  as  I  have  previously  mentioned,  advisable.  Should 
it  fail,  an  attempt  may  be  made  to  prevent  rupture  by  sup- 
porting the  tumour  externally  by  means  of  a  pad  of  felt,  tin, 
or  other  material. 

COARCTATION    OF   THE    THORACIC   AORTA. 

Etiology  and  Pathology. — Cases  are  occasionally  met  with, 
but  none  have  come  under  my  own  observation,  in  which  the 
thoracic  aorta  is  constricted  just  beyond  the  point  at  which 
it  is  joined  by  the  ductus  arteriosus  Botalli. 

The  constriction  seems  to  be  due  to  the  fact  that  the 
obliterative  process,  which  closes  the  ductus  arteriosus  soon 
after  birth,  passes  to,  and  involves  the  part  of  the  aorta  to 
which  the  ductus  arteriosus  is  attached.  In  some  cases,  the 
constriction  is  slight ;  in  others  great  ;  occasionally  complete. 

Pathological  physiology. — The  effect  of  the  constriction  is, 
of  course,  to  interfere  with  the  free  passage  of  the  blood  from 
the  transverse  into  the  descending  portions  of  the  aortic  arch. 
In  those  cases  in  which  the  constriction  is  considerable  or 
complete,  the  descending  portion  of  the  thoracic  and  the 
abdominal  aorta  and  their  branches  have  to  be  supplied 
in  a  circuitous  or  roundabout  manner  ;  the  innominate 
and    left    subclavian    arteries,    the    deep-seated    arteries    of 


Coarctation  of  the  TJioracic  Aorta. 


7A7 


(/•>vw  ll'alslw,  after 


npubliihi;d  draiviiii:^  by  Cats-jrc//.) 


Fig.  297.  a,  pulmonary  arterj' ;  b,  arterial  duct  ;  c,  arch  of  aorta  ;  </,  coarctation 
of  aorta  ;  e,  descending  aorta  ;  f,  innominate  artery  ;  g,  internal  mammary  artery; 
//,  epigastric  artery  ;  i,  i,  i,  i,  deep-seated  arteries  of  neck  and  intercostals,  form- 
'"&>  together  with  the  internal  mammary  and  epigastric  arteries,  a  collateral  circu- 
lation with  the  thoracic  and  abdominal  aorta  and  internal  iliacs. 

V\c,.  298.   Aorta  laid  open,  showing  by  probe  the  amount  of  constriction. 


tile  neck,  the  superior  intercostal,  internal  mammary,  and 
epigastric  arteries  become  enormously  enlarged,  and  the 
circulation  is  carried  on  through  the  inosculations  which  are 
so  well  represented  in  figs.  297  and  298. 


748  Diseases  of  the  Heart. 

Symptoms. — In  those  cases  in  which  the  constriction  is 
slight,  there  may  be  no  symptoms.  When  the  constriction  is 
great,  dyspnoea,  cough,  haemoptysis,  and  vertigo,  are  the  chief 
symptoms  which  hav^e  been  observed. 

Pliyskal  signs. — The  passage  of  the  blood  through  the 
constricted  portion  of  the  aorta  generates  a  murmur,  which  is 
post-systolic  rather  than  systolic,  is  extensively  propagated 
down  the  course  of  the  aorta,  and  does  not  exactly  corre- 
spond to  any  of  the  ordinary  systolic  murmurs  generated 
within  the  heart. 

The  most  characteristic  indication  of  the  condition  is, 
however,  the  enlargement  of  the  vessels  arising  from  the 
aortic  arch,  and  of  the  intercostal  and  epigastric  arteries, 
through  which  the  anastamotic  circulation  is  carried  on  ;  in 
consequence  of  this  enlargement,  pulsation,  which  is  some- 
times so  great  as  to  suggest  the  presence  of  an  aneurism  of 
the  innominate  or  transverse  portion  of  the  aortic  arch,  is 
observed  at  the  root  of  the  neck.  '  Occasionally,'  according 
to  Walshe,  '  local  expansile  impulse,  aneurismal  to  the  feel 
(and  sometimes  strong  enough  to  gradually  wear  away  the 
ribs),  may  be  felt  from  place  to  place  in  the  latter  (intercostal) 
vessels.'  ^  Thrills  and  murmurs  can  usually  be  heard  over 
the  enlarged  arteries. 

Diagnosis. — The  condition  has  seldom  been  suspected, 
much  less  recognised,  during  life.  The  slighter  forms  of  con- 
striction cannot  be  positively  diagnosed.  When  the  con.- 
striction  is  great,  and  when  enlargement  of  the  intercostal 
and  epigastric  arteries  can  be  recognised  during  life,  the 
diagnosis  would  be  easy.  In  those  cases  in  which  the  great 
vessels  arising  from  the  arch  of  the  aorta  are  much  dilated, 
aneurism  may  be  simulated. 

Prognosis. — A  slight  amount  of  constriction  is  not  incom- 
patible with  a  long  life ;  the  prognosis  in  the  more  severe 
forms    is   very    uncertain  ;    in    some  cases   the    patient    dies 

'  Diseases  of  the  Heart,  p.  536. 


Coarctation  of  the  TJioracic  Aorta.  749 

suddenly  from  rupture  of  the  aorta,  or  one  of  its  dilated 
branches ;  in  others,  in  consequence  of  the  secondary  altera- 
tions, such  as  cardiac  dilatation,  which  arc  produced  in  the 
heart,  or  parts  of  the  circulation  behind  the  left  heart  {i.e.  the 
lungs,  right  heart,  etc.);  in  others  again,  from  acute  inflam- 
matory changes  in  the  heart  or  aorta. 

Treatment. — The  main  objects  of  treatment  are  to  keep 
the  circulation  as  quiet  as  possible,  and  to  avoid  exposure  to 
cold  and  other  conditions  likely  to  induce  acute  inflammatory 
changes  in  the  heart  and  aorta.  When  symptoms  of  mechani- 
cal derangement  of  the  circulation  arise,  they  must  be  treated 
in  accordance  with  their  nature  and  the  special  indications  in 
each  case. 

For  further  details  of  this  interesting  but  rare  condition 
the  reader  is  referred  to  Dr  Walshe's  description,^  to  which  I 
am  largely  indebted  for  the  foregoing  account  of  the  disease. 

'  Diseases  of  /he  Heart,  p.  533. 


APPENDIX. 


THE  EXAMINATION  OF  THE  HEART  BY  MEANS  OF  THE 
CARDIOGRAPH. 

By  means  of  the  cardiograph  it  is  possible,  in  many  cases,  to 
obtain  a  graphic  record  of  the  cardiac  impulse  ;  and  the 
information,  which  this  method  of  examination  affords,  is 
sometimes  of  considerable  diagnostic  value. ^ 

Cardiographic  tracings  are  usually  obtained  from  the 
pulsations  of  the  left  apex-beat,  for  the  cardiac  impulse  is,  as 
a  rule,  better  defined  at  this  point  on  the  surface  of  the  chest 
than  at  any  other  ;  and  since  the  apex-beat  (i.e.  the  left  apex- 
beat)  is  due  to  the  impulse  of  the  ventricles,  more  especially 
of  the  left  ventricle,  against  the  chest  wall,  it  follows  that 
tracings  taken  from  the  apex-beat  represent  the  alterations 
which  take  place  in  the  ventricles  (more  especially  in  the 
left  ventricle)  during  the  cardiac  cycle. 

The  infonnation  zvJiich  may  be  derived  from  the  cardio- 
graph. By  means  of  the  cardiograph  we  are  able,  in  some 
cases  of  cardiac  disease  (but  not  in  all)  to  obtain  a  graphic 
record  of  the  condition  of  the  ventricles  (more  especially  of 
the  left  ventricle)  during  their  systole  and  diastole,  and  to 
determine  : — 

(i.)  The  relative  duration  of  the  ventricular  systole  and 
diastole. 

(2.)  The  manner  in  which  the  ventricular  systole  is  being- 
carried  out. 

(3.)  The  manner  in  which  the  ventricles  are  being  filled 
with  blood  during  their  diastole. 

'  The  description  of  the  cardiograph  has  not  been  included  in  the  text,  for  the 
instrument  is  rarely  used  even  in  hospital  practice,  and  cannot,  as  yet,  be  said  to 
be  one  of  the  ordinary  means  of  clinical  investigation. 


752  Appendix. 

Since  the  filling  of  the  ventricles  to  a  large  extent  depends 
upon  the  condition  of  the  auriculo-ventricular  orifices  and  of 
the  auricular  contractions  {i.e.  of  the  muscular  wall  of  the 
auricles),  the  cardiograph  affords  in  some  cases  : — 

(4.)  Information  as  to  the  condition  of  these  parts  (more 
especially  of  the  condition  of  the  mitral  orifice  and  the 
muscular  wall  of  the  left  auricle). 

Further,  by  means  of  the  cardiograph  it  is  possible 
to  clear  up  some  obscure  cases  of  cardiac  disease,  and  to 
ascertain  the  exact  relationship  of  murmurs  (which  it  is 
difficult  or  impossible  to  '  time '  in  any  other  way)  to  the 
different  periods  of  the  cardiac  cycle. 

By  comparing  tracings  taken  from  successive  beats  of 
the  heart  (subject  to  the  precautions  which  will  be  presently 
described),  the  presence  of  inequalities  and  irregularities  in 
the  cardiac  action  can  be  graphically  demonstrated. 

The  cardiograph  is,  however,  in  many  cases  an  unsatis- 
factory instrument  to  work  with, — much  less  satisfactory  than 
the  sphygmograph.  The  button  of  the  sphygmograph  can, 
with  rare  exceptions,  be  speedily  and  easily  applied  so  as  to 
exert  direct  pressure  upon  the  radial  artery,  and  the  tracing 
which  is  thus  obtained  is  an  accurate  representation  of  the 
alterations  which  take  place  in  the  vessel,^  but  it  is  often 
difficult  or  impossible  to  obtain  a  cardiographic  tracing,  for 
the  apex-beat  is  sometimes  very  feeble,  or  altogether  effaced  ; 
the  tracings  which  are  obtained  are  often  inverted,  and  there- 
fore unreliable.  Even  good  tracings  are  difficult  to  analyse, 
for  they  represent  not  only  the  alterations  in  the  size  and  state 
of  the  ventricles  (more  especially  of  the  left  ventricle)  which 
result  from  the  contraction  and  relaxation  of  their  muscular 
walls,  and  from  the  collapse  which  attends  the  emptying,  and 
the  distention  which  results  from  the  filling  of  their  cavities ; 
but  also  the  movements  of  the  heart  as  a  whole,  for  every 
alteration  in  the  heart  (or  the  surrounding  parts)  which  pushes 

'  The  radial  artery  at  the  lower  end  of  the  radius  is  quite  superficial, 
and  rests  upon  bone ;  in  most  cases,  therefore,  it  can  be  directly  compressed 
between  the  button  of  the  sphygmograph  and  the  flat  surface  of  the  radius  on 
which  it  lies. 


Forms  of  Cardiographs.  753 

it  against,  or  causes  it  to  recede  from,  the  front  wall  of  the 
chest,  produces  alterations  in  the  character  of  the  cardiac 
impulse.  The  force  and  character  of  the  apex  pulsation 
depend  in  fact,  to  a  very  large  extent,  upon  the  condition  of 
the  anterior  margin  of  the  left  lung  (whether  distended  during 
inspiration  or  retracted  during  expiration)  ;  while  the  move- 
ments of  the  chest  wall  which  attend  inspiration  and  expira- 
tion, and  the  influence,  which  the  acts  of  inspiration  and 
expiration  have  on  the  blood-pressure  within  the  cardiac 
cavities,  are  actively  manifested  in  the  cardiographic  tracing. 
It  must  be  remembered  then,  that  cardiographic  tracings  do 
not  represent  in  such  a  simple  and  accurate  manner  the  altera- 
tions which  are  taking  place  within  the  heart,  as  sphygmo- 
graphic  tracings  represent  the  alterations  which  are  going  on 
within  the  radial  artery. 

FORMS    OF    CARDIOGRAPHS. 

I.  Galabins  Cardiograph  (see  fig.  299),  which  probably 
gives  the  most  reliable  tracings,  is  simply  a  modification  of 
Marey's  Sphygmograph. 

Dr  Galabin's  description  of  it  is  as  follows^: — 'The  brass 
frame  of  the  instrument  resembles  that  of  the  sphygmograph, 
except  as  regards  the  bar  which  carries  the  knife  edge,  A, 
through  which  the  motion  is  transmitted  to  the  long  lever. 
This  bar,  B,  is  made  up  of  two  parts,  of  which  one  slides 
within  the  other,  and  can  be  fixed  by  means  of  a  screw,  C,  in 
whatever  position  is  desired.  There  is  also  a  second  knife 
edge,  D,  which  can  be  raised  or  lowered  at  pleasure,  attached 
to  the  same  bar  at  a  greater  distance  from  the  axis  of  the 
long  lever.  By  this  means  the  magnifying  power  of  the 
instrument,  as  regards  the  vertical  height  of  the  curve  de- 
scribed, can  be  varied  from  ten  to  about  a  hundred.  The 
brass  frame,  which  in  the  sphygmograph  is  rigidly  fixed  to 
two  parallel  bars  of  ivory  by  which  it  is  supported,  is  freely 
suspended  in  the  cardiograph  by  means  of  two  transverse  rods 
of  steel,  E.  These  are  attached  by  joints,  F,  which  allow  both 
of  vertical  and  horizontal  adjustment,  to  four  vertical  rods  of 

'  Mcdico-Cliiritrgical  Ti-atisactions,  vol.  Iviii.  p.  359. 
B  B  B 


754 


Appendix. 


s 


Galabiiis  CardiograpJi.  755 

steel,  G,  each  pair  of  which  is  inserted  into  a  bar  of  wood 
covered  with  leather, — by  means  of  these  wooden  bars  the 
instrument  rests  upon  the  chest.  They  can  be  separated  to  a 
width  of  nearly  five  inches,  and  the  instrument  can  be  raised 
or  lowered  at  pleasure  at  either  end,  and  in  this  way  it  can 
be  adapted  to  a  chest  of  any  size  or  shape. 

'In  order  that  vertical  adjustments  at  either  end  may  be 
possible  independently,  the  brass  frame  is  not  in  immediate 
contact  with  both  the  transverse  bars  which  support  it,  but 
at  one  end  it  is  suspended  by  an  intermediate  piece  of  brass,  I, 
which,  when  the  instrument  is  in  position,  is  tightened  and 
made  rigid  by  a  screw.  The  spring  which  is  employed  to 
press  upon  the  centre  of  impulse  is  arranged  in  a  mode  similar 
to  that  adopted  in  the  sphygmograph.  The  mechanism,  how- 
ever, by  which  the  amount  of  pressure  is  finally  adjusted  is  a 
simpler  one  than  that  employed  in  any  one  of  the  various 
forms  of  sphygmograph  now  generally  used.  This  simplifica- 
tion is  rendered  possible  by  the  fact  that,  in  the  case  of  cardio- 
graphic  tracings,  a  knowledge  of  the  exact  amount  of  pressure 
employed  would  have  little  or  no  significance.  The  adjust- 
ment is  effected  by  means  of  a  screw,  K,  which  perforates  the 
short  arm  of  the  spring  lever,  B.  The  weight  of  the  lever 
itself  is  also  counterbalanced  by  a  small  antagonistic  spring. 

'In  this  way  the  pressure  upon  the  point  at  w^hich  the 
spring  pad  is  applied  can  be  reduced  almost  to  zero,  and 
thus  it  is  easy  to  obtain  with  this  instrument  a  tracing  repre- 
senting the  backstroke  in  veins  which  even  the  weight  of  the 
spring  of  an  ordinary  sphygmograph  is  generally  sufficient 
to  extinguish. 

'  There  are  also  two  small  springs,  L,  of  different  strength, 
to  depress  the  long  lever  and  prevent  its  being  jerked  away 
by  any  sudden  motion  from  the  knife  edge  on  which  it  rests. 
Either  of  these  can  be  used  or  turned  aside  at  pleasure.  When 
the  instrument  is  used  in  a  vertical  position  it  is  generally 
better  to  dispense  with  this  small  spring,  since  it  adds  a  little 
to  the  friction,  and  it  is  found  that  the  lever  does  not  become 
separated  from  the  knife  edge,  provided  that  the  magnifying 
power  of  the  cardiograph  be  so  adjusted  that  its  movements 


756 


Appendix. 


have  only  a  very  moderate  amplitude.  If,  however,  it  is 
desired  to  take  a  tracin.s:  from  a  patient  in  a  sitting  or  standing 
posture,  it  is  necessary  to  use  the  secondary  spring,  for  then 
the  recording  lever  is  no  longer  kept  in  position  by  its  own 
gravity. 

'  The  cardiograph  may  be  fixed  upon  the  chest  by  two 
narrow  straps  passed  round  the  bod}^  and  fastened  by  buckles. 
These  should  be  partly  elastic,  that  they  may  yield  a  little  if 
the  patient  makes  an  inspiratory  effort  while  the  clockwork 
is  in  motion.  In  this  way  the  disturbing  influence  of  the 
muscular  movement  upon  the  cardiac  curve  is  diminished. 
As  soon,  however,  as  the  observer  has  acquired  some  dexterity, 
it  will  be  found  sufficient  in  most  instances  to  hold  the  instru- 
ment against  the  chest  with  the  hand.' 

2.  Marey's  Cardiograph  and  its  modifications. — Marey's 
cardiograph  consists  of  two  tambours  connected  by  means  of 
a  flexible  hollow  tube.     A  button,  which  is  attached  to  one 


Fig.   300. — Mareys  Taiiilour. 

The  metal  chamber  i)i  is  covered  in  an  air-tight  manner  with  the  india-rubber 
r,  bearing  a  thin  metal  plate  in'  to  which  is  attached  the  lever  /  moving  on  the 
hinge  h.  The  whole  tambour  can  be  placed  by  means  of  the  clamp  cl  at  any 
height  on  the  upright  s' .  The  indiarubber  tube  t  serves  to  connect  the  interior 
of  the  tambour  to  which  the  lever  is  attached  with  the  cavity  of  the  tambour 
which  is  placed  over  the  apex-beat. 


Directions  for  taking  a  Cardiographic  ti'acing.    757 

of  the  tambours,  is  accurately  applied  over  the  position  of  the 
apex-beat  ;  to  the  second  tambour  the  recording  lever  is 
attached.  (See  fig.  300.)  Any  impulse  communicated  to 
the  button  of  the  first  tambour  drives  the  air  out  of  it,  and 
through  the  connecting-tube  to  the  second  tambour  ;  the 
alterations  which  are  produced  in  the  second  tambour  in  this 
manner,  are  communicated  to  the  writing  lever,  which  records 
the  tracing  on  a  piece  of  smoked  paper  attached  to  a  revolving 
cylinder  called  a  polygraph. 

3.  The  ordinary  Sphygmograpk. — In  some  cases  in  which 
the  apex-beat  is  very  distinctly  localised,  cardiographic  tracings 
may  be  obtained  by  means  of  the  ordinary  sphygmograph. 
In  the  majority  of  cases  of  cardiac  disease  the  impulse  is  too 
diffused  to  permit  of  the  satisfactory  use  of  Marey's  sphygmo- 
graph for  this  purpose,  for  the  shock  of  the  heart  is  com- 
municated to  the  framework  as  well  as  to  the  button  of  the 
instrument  and  the  tracing  is  consequently  unreliable.  Dr 
Sansom  frequently  uses  Pond's  sphygmograph  as  a  cardio- 
graph. 

DIRECTIONS   FOR   TAKING   A   CARDIOGRAPHIC   TRACING. 

1.  Place  tJie  patient  in  tlie  proper  position.— \{  possible  he 
should  be  placed  on  his  back  in  bed  ;  unfortunately  in  many 
cases  a  cardiographic  tracing  cannot  be  obtained  in  this  posi- 
tion, for  when  the  cardiac  impulse  is  feeble  it  may  be  necessary 
to  make  the  patient  sit  up  or  lean  forward  in  order  to  get  an 
apex-impulse  of  sufficient  power  to  produce  a  cardiographic 
tracing ;  again,  in  many  cases  of  cardiac  disease,  the  patient 
is  unable,  on  account  of  shortness  of  breath,  to  lie  in  the 
recumbent  position.  When  a  cardiographic  tracing  is  taken 
by  means  of  Galabin's  instrument  with  the  patient  in  a  sitting 
position,  the  small  secondary  spring  (L)  must  be  used  in  order 
to  keep  the  writing  lever  in  contact  with  the  turned-up  knife 
edge. 

2.  Carefully  ascertain  and  mark  the  exact  position  of  the 
maximum  point  of  pulsation  of  the  apex-beat. 

'  3.  Apply  the  instrument,  having  previously  screwed  up  the 


758  Appendix. 

clockwork  and  smoked  the  paper  and  fitted  in  tlie  slide  which 
carries  it. 

The  horizonal  adjustments  must  be  altered  so  that  the 
wooden  bars  rest  firml\-  on  the  chest-wall  beyond  the  range 
of  the  cardiac  impulse  ;  the  ivory  pad  must  be  accurately 
applied  over  the  exact  point  of  inaxiiiinin  apex-pulsation  ;  the 
vertical  adjustments  being  altered  in  order  to  permit  of  its 
accurate  application  to  the  wall  of  the  chest ;  (the  accurate 
application  of  the  ivory  pad  to  the  exact  point  of  maximum 
apex-pulsation  is  of  the  greatest  practical  importance,  for 
unless  this  point  is  attended  to,  the  tracing  is  apt  to  be  in- 
verted, and  therefore  unreliable)  ;  the  sliding  bar  must  be  so 
adapted  that  a  suitable  amount  of  movement  of  the  writing 
lever  is  obtained  (after  an)'  alteration  of  the  sliding  bar  to 
which  the  knife  edge  is  attached,  the  ivory  button  must  of 
course  be  again  carefully  reapplied  over  the  point  of  maximum 
apex-pulsation)  ;  the  instrument  is  then  fixed  to  the  chest  by 
means  of  the  straps  (tracings  maybe  obtained  by  holding  the 
instrument  in  contact  with  the  chest-wall,  but  it  is,  I  think, 
advisable,  for  the  sake  of  accuracy,  to  fix  the  instrument  and 
not  merely  to  hold  it). 

4.  Make  the  patient  expire  and  hold  his  breath,  and  ivhi/e 
he  is  Jwlding  his  breath  start  the  clockivork  and  take  the  tracing. 

This  is  also  a  point  of  the  greatest  practical  importance, 
for,  if  the  tracing  is  taken  during  the  act  of  respiration  it 
becomes  complicated,  the  cardiac  impulse  being  interfered 
with  by  the  anterior  edge  of  the  left  lung,  and  the  movements 
of  the  chest  wall  which  attend  the  act  of  respiration  being 
communicated  to  the  writing  lev^er.  It  is  of  the  utmost  im- 
portance therefore  to  take  the  tracing  during  complete  expira- 
tion (for  then  the  anterior  edge  of  the  left  lung  is  retracted, 
and  a  large  part  of  the  anterior  surface  of  the  heart  is  in 
direct  contact  with  the  chest  wall),  and  while  the  patient  holds 
his  breath  (in  order  that  the  movements  of  the  lever  may 
represent  the  cardiac  impulse  only,  and  not  be  complicated  by 
the  respiratory  movements  of  the  chest  wall).  It  must  also 
be  remembered  that  the  acts  of  inspiration  and  expiration 
materially  modify  the  condition  of  the  intra-cardiac  circulation. 


Analysis  of  a  Cardiographic  tracing.  759 

Unfortunately  these  ideal  conditions  cannot  always  be 
obtained.  In  many  cases  of  cardiac  disease  the  patient  is 
suffering  from  dyspncea,  and  is  quite  unable  to  hold  his 
breath  ;  in  others,  again,  the  lungs  are  emphysematous,  and 
during  expiration  the  greater  part,  or  even  the  whole  of  the 
anterior  surface  of  the  heart,  is  overlapped,  and  its  impulse 
therefore  obscured. 

ANALY.SIS   OF   A   CARDIOGRAPHIC   TRACING. 

The  analysis  of  cardiographic  tracings  is  attended  with 
great  difficulties,  and  some  important  points  are  not  yet 
clearly  understood.  The  conclusions,  which  have  been 
arrived  at,  have  been  partly  drawn  from  observation  (such  as 
those  of  Chauveau  and  Marey)  made  by  recording  the  pres- 
sure within  the  cardiac  cavities  of  the  lower  animals,  e.g.  the 
horse  ;  partly  from  tracings  taken  from  the  exposed  hearts  of 
the  lower  animals,  the  button  of  the  tambour  being  in  direct 
contact  with  the  exterior  of  the  ventricles  ;  and  partly  from 
cardiographic  tracings  taken  from  the  cardiac  impulse  as  felt 
on  the  chest  wall  of  men. 

A  cardiographic  tracing  consists  of  a  series  of  curves 
(see  fig.  301),  each  one  of  which  corresponds  to  a  complete 
cardiac  revolution,  i.e.  the  time  which  elapses  from  the  com- 
mencement of  one  ventricular  systole  to  the  termination  of 


Fig.    301.    N'oniia!  Cardiograpliic  tracing. — [After  Galahiii.) 

the  ventricular  diastole.  Each  individual  cardiac  curve  (see 
fig.  302  A  to  B)  is  composed  of  two  portions,  i  and  2,  which 
represent  the  systole  and  diastole  of  the  ventricles  respec- 
tively ;  and  since  cardiographic  tracings  in  man  are  usually 


76o 


Appendix. 


taken  from  the  left  apex-beat,  it  is  the  systole  and  diastole 
of  the  left  ventricle  which  is  most  accurately  represented. 
In  the  following  description  I  shall  then,  for  the  sake  of  sim- 
plicity, limit  my  remarks  to  the  left  heart.^ 


Fig.   302. — Normal  cardiographic  wave. — (Enlarged  and  modified  from  Galabin.) 

A.  B.  base  line;  i,  systolic,  and  2  diastolic  portions  of  the  tracing;  for 
the  significance  of  the  other  letters  see  text  (p.  760,  ct  seq.) 

The  systolic  portion  of  the  tracing. 

The  systolic  portion  of  the  tracing  taken  from  the  apex- 
impulse  in  man,  may  for  descriptive  purposes,  be  divided  into 
the  following  parts  : — 

1.  A  line  of  ascent  (a'  to  d). 

2.  A  summit  or  apex  (d). 

3.  A  line  of  descent  (d  to  c). 

Professor  Michael  Foster  concludes  that  the  down-stroke 
from  d  to  a  (in  fig.  303)  corresponds  to  the  relaxation  of  the 

'  In  normal  cardiographic  tracings  the  whole  of  each  individual  cardiac  curve 
or  vvfave  is  not,  as  in  the  case  of  the  normal  sphygmographic  or  pulse  curve,  situ- 
ated above  the  base  line  of  the  tracing,  i.e.  a  line  drawn  through  the  commence- 
ment of  the  up-stroke  of  succeeding  curves  or  waves ;  but  the  commencement  of 
the  up-stroke  is  situated  above  the  portion  of  the  cardiographic  curve  which 
represents  the  ventricular  diastole  (see  fig.  301).  The  hyperdicrotic  pulse  curve 
presents  the  same  character. 


Analysis  of  a  Cardiographic  tracing.  761 

ventricles,  and  if  this  interpretation  is  to  be  applied  to  trac- 
ings taken  from  the  apex-beat  of  man,  the  whole  of  the  down- 
stroke  ought  to  be  included  in  the  diastolic  and  not  in  the 
systolic  portion  of  the  tracing.  But  as  Dr  Galabin  points 
out,  the  second  sound  in  man  is  usually  heard  to  occur 
towards  the  termination  rather  than  at  the  commencement 
of  the  line  of  descent,  and  if  this  is  so,  and  if,  as  Professor  M. 
Foster  points  out,  '  at  the  actual  closure  of  the  semilunar 


Fig.  303. — 'Normal  heart  curve  showing  changes  in  the  antero-posterior 
diameter  of  the  ventricle  obtained  from  the  cat  by  a  light  recording  lever  moved 
by  a  button  which  pressed  gently  on  the  anterior  surface  of  the  ventricle.  The  time 
curve  gives  50  double  vibrations  per  second,  and  lines  have  been  drawn  to  show 
the  duration  of  the  different  phases  of  the  ventricular  movement,  a  {o  l>  corre- 
sponds to  the  distension  of  the  ventricle  including  the  auricular  systole,  the  wave- 
like rise  during  this  period  being  due  to  the  increase  in  the  diameter  of  the  ventricle 
resulting  from  the  entrance  into  it  of  the  contents  of  the  auricle.  The  period 
from  (^  to  r  corresponds  to  the  time  from  the  commencement  of  the  ventricular 
contraction  to  the  moment  when  the  organ  has  completed  its  change  in  shape 
from  a  flattened  to  a  more  rounded  form.  The  highest  part  of  the  curve  corre- 
sponds also  in  time  with  the  opening  of  the  semilunar  valves  as  well  as  the  firm 
closure  of  the  auriculo-ventricular  valves.  The  duration  of  this  period  in  this  case 
is  only  about  3-5oths  of  a  second.  The  period  from  c  to  d  is  that  during  which  the 
ventricle  having  grasped  its  contents  is  emptying  its  cavity  and  remaining  con- 
tracted. It  can  be  seen  that  only  during  the  first  half  of  this  period  is  there  any 
marked  descent  of  the  lever  point ;  in  other  words,  the  antero-posterior  diameter 
does  not  continue  to  diminish  during  the  whole  period  of  the  systole,  indicating 
that  little  or  no  blood  was  thrown  out  during  the  second  half  of  this  period,  the 
ventricle  remaining  simply  contracted  after  having  emptied  its  cavity.  The 
period  from  ^  to  a  is  that  during  which  the  ventricular  muscle  is  relaxing.  Here, 
as  is  frequently  the  case,  there  is  no  period  of  pause  between  the  close  of  the 
relaxation  of  the  ventricle  and  the  commencement  of  the  succeeding  distension. 
The  tracing  gives  no  evidence  as  to  the  time  of  closure  of  the  semilunar  valves.' — 
(  Text- Book  of  Physiology,  by  Professor  AI.  Foster,  fourth  edition,  p.  147.) 


762 


AppcndL\ 


valves,  giving  rise  to  the  second  sound,  the  ventricle  has 
just  finished  its  systole  and  is  beginning  to  relax,'  it  would 
appear  that  during  the  commencement  of  the  down-stroke 
the  ventiicles  are  still  in  systole. 

The  tracings  of  Chauvcau  and  Marey,  represented  in 
fig.  304,  afford,  I  think,  some  corroboration  of  this  view.  It 
will  be  seen  by  reference  to  the  figure  that  the  down-stroke 
of  the  third  tracing,  taken  from  the  outside  of  the  chest,  is 
already  considerably  advanced  before  the  sudden  descent  of 
the  intra-vcntricular  pressure,  which  marks  the  relaxation  of 
the  ventricles  (in  the  second  tracing),  occurs. 


Fig.  304. — Simultaneous  /racings,  from  the  interior  of  the  right  auricle,  from  the 
interior  of  the  right  ventricle,  and  of  the  cardiac  impulse  in  the  horse. 
{After  Chauveau  and  Marey.)     To  he  read fro7n  left  to  right. 

The  upper  curve  represents  changes  taking  place  within  the  auricle,  the  middle 
curve,  changes  within  the  ventricle.  The  lower  curve  represents  the  variations  of 
pressure  transmitted  to  a  lever  outside  the  chest  and  constituting  the  cardiac 
impulse.  A  complete  cardiac  cycle,  beginning  at  the  close  of  the  ventricular 
systole,  is  comprised  between  the  thick  vertical  lines  I.  and  II.  The  thin  vertical 
lines  represent  tenths  of  a  second. 

TJic  line  of  ascent  or  upstroke  (a'  to  d,  figs.  301  and  302) 
represents  the  impulse  which  is  produced  against  the  chest- 
wall  by  the  rounding  and  hardening  of  the  walls  of  the  ven- 


Analysis  of  a  CavdiograpJiic  tracino.  763 

tricle  which  attend  the  commencement  of  the  ventricular 
systole.  The  contraction  of  the  ventricle,  therefore,  com- 
mences suddenly. 

The  commencement  of  the  up-stroke  slightly  precedes  the 
first  sound  of  the  heart  which  occurs  during  the  ascent  of  the 
lever  (a  fact  whicn  is  determined  by  listening  to  the  heart 
sounds  and  watching  the  exact  position  of  the  lever  of  the 
cardiograph  when  the  first  sound  occurs),  and  which  reaches 
its  maximum  intensity  as  the  lever  approaches  the  summit 
of  the  up-stroke.  The  closure  of  the  auriculo-ventricular 
valves  (the  sudden  tension  of  which  is,  as  we  have  previously 
seen,  the  main  cause  of  the  first  sound  of  the  heart)  occurs, 
therefore,  during  the  up-stroke.  In  some  tracings  the  up- 
stroke is  not  quite  straight,  but  is  broken  by  a  slight  interrup- 
tion or  wave  {b)  (see  fig.  305)  which  is  supposed  to  indicate 
the  closure  of  the  auriculo-ventricular  valves.  This  wave  is 
only  occasionally  present. 


Fig.  305.  —  Cardiographic  tracing  from  a  case  of  aortic  obstrtiction  avd  regurgita- 
tion, with  some  mitral  regin-gitation,  showiitg  the  ivave  h,  ichich  is  supposed 
to  indicate  closure  of  the  miti-al  valve. — {After  Sansom. ) 

The  closure  of  the  auriculo-ventricular  valves  '  might  be  expected,' 
says  Dr  Galabin,  '  to  produce  first,  a  slight  check,  and  then  an  accelera- 
tion in  the  ascent  ;  the  check,  due  to  the  shock  of  the  blood  against  the 
valves  impelHng  the  heart  in  the  direction  of  its  base  ;  the  acceleration, 
in  consequence  of  the  increased  hardening  of  the  ventricle  as  soon  as  it 
meets  with  resistance.' ' 

The    opening    of    the    aortic    valves    corresponds  to    the 
summit  of  the  up-stroke  or  line  of  ascent  {d),  and  is  separated, 

'   Guys  Hospital  Reports  1875,  p.  274. 


764  Appendix. 

therefore,  from  the  commencement  of  the  hardening  of  the 
walls  of  the  ventricle  by  a  distinct  interval.^ 

With  the  opening  of  the  aortic  valve  there  is,  as  we  would 
expect,  a  fall  of  the  lever  corresponding  to  the  relief  which  is 
afforded  to  the  ventricle  by  the  discharge  of  the  first  portion 
of  its  contents  into  the  aorta.  This  fall  is  most  marked  when 
the  ventricle  contracts  suddenly,  and  when  the  resistance  to 
the  opening  of  the  valve  is  slight ;  vice  versa  it  is  least  marked 
when  the  ventricle  contracts  slowly,  and  when  there  is  a  con- 
siderable obstruction  to  the  passage  of  the  blood  from  the 
ventricle  into  the  aorta.  The  obstruction  may  be  situated 
at  the  aortic  orifice  (as  in  stenosis),  or  in  the  peripheral 
vessels  (as  in  chronic  Bright's  disease).  The  apex  wave  is 
probably  also  in  part  due  to  the  inertia  of  the  instrument. 
In  the  tracing  taken  directly  from  the  ventricle  of  the  cat 
(see  fig.  303)  the  descent  of  the  lever,  after  the  bursting  open 
of  the  aortic  valve,  is  seen  to  be  very  slight. 

After  the  aortic  valve  has  been  opened,  the  ventricle,  under 
normal  circumstances,  continues  to  contract  for  a  considerable 
time.  In  tracings  taken  directly  from  the  exterior  of  the 
ventricle  (as  in  fig.  303),  the  period  is  probably  represented, 
as  Dr  M.  Foster  points  out,  by  the  portion  of  the  tracing 
which  is  included  between  the  letters  c  and  d.  In  tracings 
taken  from  the  apex-impulse  of  man,  the  ventricular  systole 
probably  also  includes  (as  has  been  previously  pointed 
out)  a  portion  of  the  subsequent  down  stroke  {d  to  g  in 
fig.  302.) 

During  the  first  part  of  this  period  {i.e.  the  part  of  the 
tracing  which  immediately  follows  c  in  fig.  303,  and  d  in 
fig.  302),  the  blood  is  being  expelled  into  the  aorta  ;  during 
the  last  part  of  the  period  (the  part  of  the  trace  immediately 
preceding  d  in  fig.  303,  and  g  in  fig.  302)  the  ventricle  is 
empty,  but  still  in  a  state  of  contraction. 

A  well  marked  wave  (/)  precedes  the  sudden  descent  of 
the  lever  in  the  normal  cardiographic  tracing  from  the  apex 

'  The  apex  {d),  of  course,  also  represents  the  opening  of  the  pulmonary  valve, 
which  event  is,  under  normal  circumstances,  synchronous  with  the  opening  of  the 
aortic  segments. 


Analysis  of  a  Cardiographic  tracing.  765 

beat  of  man  (see  figs.  301  and  302),  but  is  not  so  well  marked 
in  the  tracing  taken  directly  from  the  ventricle  of  the  cat. 
(See  fig.  303.)  Its  exact  significance  is  not  definitely  deter- 
mined. Dr  Galabin  thinks  that  it  is  due  to  the  locomotion 
of  the  heart  as  a  whole.^  Dr  Sansom  is  of  opinion  that  the 
wave  represents  forcible  distention  of  the  aorta  at  the  end  of 
the  ventricular  systole,^ 

Between  the  apex  of  the  up-stroke  {d)  and  the  curve  (/"),  a 
small  wave  {e)  is  sometimes  seen.  Observers  are  not  agreed 
as  to  its  exact  significance  ;  possibly  it  may,  I  think,  represent 
the  resistance  which  the  ventricle  meets  with  (or  rather  the 
powerful  contraction  which  is  necessitated  on  the  part  of  the 
ventricle)  as  it  forces  the  blood  into  the  arterial  system,  after 
the  aortic  valve  has  been  opened. 

The  exact  point  in  the  tracing  which  marks  the  closure 
of  the  aortic  valves  is  difficult  to  determine,  and  is  not  yet 
definitely  settled.  Professor  M.  Foster  states  with  regard  to 
this  point,  '  Hence  we  may  infer,  and  the  conclusion  may  be 
supported  by  other  arguments,  that  at  the  actual  closure  of 
the  semilunar  valves,  giving  rise  to  the  second  sound,  the 
ventricle  has  just  finished  its  systole  and  is  beginning  to 
relax.  If  this  view  be  correct,  the  time  of  the  closure  of  the 
valves  is  not  indicated  on  the  cardiographic  tracing  by  any 
special  mark,  but  coincides  with  the  commencement  of  the 
sudden  fall  of  the  lever,'^  as  at  d  in  fig.  303. 

If  we  include  a  portion  of  the  line  of  descent  in  the  systolic 
portion  of  the  tracing,  the  closure  of  the  aortic  valves  should 
occur  near  the  termination,  rather  than  at  the  commencement, 
of  the  line  of  descent ;  and  in  support  of  this  view  Dr  Galabin 
states  that  under  normal  circumstances,  and  more  especially 
when  the  arterial  blood  pressure  is  low,  the  second  sound  can 

'  In  speaking  of  this  wave  Dr  Galabin  says,  'Thus  we  see  that /"corresponds 
in  time  to  the  maximum  contraction  of  the  ventricle.  Since,  however,  when  it 
takes  the  form  of  an  elevation  in  the  positive  tracing,  it  cannot  be  due  to  the  con- 
traction of  the  ventricle  as  such;  its  cause  must  be  sought  in  some  coincident 
occurrence,  and  this  can  only  be  the  locomotion  of  the  heart  as  a  whole.' — {Guy's 
Hospital  Reports,  1875,  p.  270.) 

•  Diat(}iosis  of  Diseases  of  the  Heart,  p.  257. 

^  Text  Book  of  Physiology,  four'h  edition,  p.  150. 


766  Appendix. 

be  heard  to  occur  towards  the  termination  rather  than  at  the 
commencement  of  this  portion  of  the  tracing.  He  concludes 
and,  with  his  opinion,  Dr  Sansom  also  agrees,  that  the  slight 
notch  g,  which  is  seen  in  some  tracings  (more  especially  when 
the  arterial  pressure  is  low),  '  if  not  produced  in  the  instrument 
may  indicate  the  moment  at  which  the  valves  close.' ^ 

When  the  blood  pressure  in  the  aorta  is  high,  the  second 
sound  is  heard  to  occur  near  the  commencement,  rather  than 
near  the  termination  of  the  line  of  descent,  and  it  is  not 
unreasonable  to  conclude  that  under  such  circumstances  the 
aortic  segments  are  closed  before  the  relaxation  of  the  ven- 
tricle has  fairly  commenced.  In  cases  of  this  description 
{i.e.  high  arterial  tension)  the  wave^  is  not  seen  in  the  tracing. 

(The  wave^  does  not,  it  must  be  observed,  correspond  to 
the  waves  e,  e,  e",  in  fig.  304,  which,  as  Professor  M,  Foster 
very  forcibly  points  out,  can  hardly,  as  has  been  supposed, 
represent  the  closure  of  the  aortic  valves.) 

To  sum  up,  then,  the  systolic  portion  of  the  cardiographic 
tracing  of  man,  which  commences  at  the  point  a'  in  fig.  302, 
probably  includes  a  portion  of  the  line  of  descent  (fto  c)  and 
probably  terminates  somewhere  about  the  point  g;  the  closure 
of  the  aortic  valves  is  probably  represented  by  the  notch  g 
which  occurs  in  some  tracings,  more  especially  when  the 
arterial  blood-pressure  is  low  ;  the  line  of  ascent  {a  to  d) 
corresponds  to  the  contraction  and  rounding  of  the  ven- 
tricles ;  the  apex  {d)  to  the  bursting  open  of  the  aortic 
valves  ;  the  wave  {b)  probably  represents  the  closure  of  the 
auriculo-ventricular  valves  ;  the  wave  {e)  possibly  represents 
the  resistance  which  the  left  ventricle  meets  with  in  propelling 
its  blood,  after  the  aortic  valves  have  been  opened,  into  the 
arterial  system  ;  the  wave  (/)  is  probably  due  to  the  move- 
ment of  the  heart  as  a  whole,  and  probably  represents  the 
distention  of  the  aorta  which  accompanies  the  emptying  of 
the  left  ventricle. 

The  summit  of  the  systolic  portion  of  the  tracing  {d  to/) 
is  broad  and  sustained  in  hypertrophy  ;  narrow  and  sharp 
in  dilatation  and  in  all  conditions  in  which  the  contraction  of 

'   Guy  s  Hospital  Reports,  1S75,  p.  274. 


Analysis  of  a  Cardiographic  tracing,  767 

the  left  ventricle  is  sharp,  short  and  unsustained  in  conditions 
therefore  of  cardiac  failure.       (See   fis^s.   306,   307   and    308.) 


Fig.  ^06. 


Fig.  307. 


Fig.  247. — Cardiogi-apliic  tracing  in  liypertrophy  Oj   the  left  ventricle.      {Aftet 

Galabin. ) 

'  Emily  L.,  tet.  8.  Loud  systolic  murmur  at  the  apex,  preceded  by  a  very  faint 
rumbling  sound.  A  presytolic  murmur  has  been  heard  previously.  Heart  much 
hypertrophied,  P.  96.'     {Guy s  Hospital  Reports,  1875,  p.  313.) 

Fig.  248.  —  Cardiographic  tracing  in  liypertrophy  of  the  left  ventricle. — {After 

Galabin. ) 

'  Thomas  G. ,  a;t.  56.  Chronic  Bright's  disease  with  atheromatous  arteries. 
The  cardiac  impulse  was  very  powerful,  but  no  murmur  was  heard,  P.  63.' — {Guy's 

Hospital  Reports,   1875,  p.  312.) 


Fig.  308. — CarJiogra/n  in  a  case  of  exophthalmic  qoitre.  —  {After  Galabin.) 

'Rebecca  S.,  set.  20.  Mitral  regurgitation  combined  with  exophthalmic 
goitre.  Heart  dilated  and  hypertrophied.  Pulse  wo.'— {Guy  s  HospUal  Reports, 
1875,  p.  314). 

In  addition,  a  series  of  irregular  (serrated)  curves  is  seen  in 
the  systolic  portion  of  the  tracing,  in  some  cases  in  which 
rough  systolic  murmurs  can  be  heard,  or  systolic  thrills  felt, 
over  the  praecordial  region. 


768  Appendix. 

The  diastolic  portion  of  t lie  tracing. 
Under  normal  circumstances  the  diastole  of  the  ventricle 
commences  with,  or  more  accurately  just  before,  the  closure 
of  the  aortic  valves,  which  event  is,  as  we  have  seen,  probably 
represented  in  some  tracings  by  the  notch  g.  At  the  com- 
mencement of  the  ventricular  diastole,  the  elastic  recoil  or 
expansion  of  the  ventricle  occurs,  the  mitral  valve  is  burst  open, 
and  blood  flows  from  the  left  auricle  into  the  left  ventricle  ; 
the  auricular  contraction  or  systole  then  occurs,  and  is  almost 
immediately  succeeded  by  the  contraction  of  the  ventricle. 

Now,  by  observing  the  character  of  the  diastolic  portion 
of  the  tracing  (the  part  numbered  2  in  fig.  302)  we  obtain 
information  as  to  the  manner  in  which  the  ventricle  is  being 
filled,  and  since  the  filling  of  the  left  ventricle  depends  to  a 
large  extent  upon  the  condition  of  the  mitral  orifice,  we 
obtain,  in  some  cases,  information  as  to  the  condition  of  that 
valvular  orifice.  Further,  we  are  able,  in  some  cases,  to  note 
the  character  of  the  auricular  contraction,  and  so  to  form  a 
judgment  as  to  the  condition  of  the  auricular  muscle.  If  we 
grant  that  the  closure  of  the  aortic  valve  occurs  towards  the 
termination  of  the  line  of  descent  from  /  to  c,  the  diastolic 
portion  of  the  tracing  may  be  said  to  be  represented,  under 
normal  circumstances,  by  a  slow  and  gradual  ascent  inter- 
rupted by  two  or  three  small  waves  {k,  I,  and  a). 

When  the  blood-flow  into  the  ventricle  is  unusually  rapid, 
as  it  is  for  instance  in  free  regurgitation  through  the  aortic 
or  mitral  orifices,  and  more  especially  when  both  aortic  and 
mitral  regurgitation  are  present,  the  line  of  ascent  which 
marks  the  diastolic  filling  of  the  ventricles  is  much  more 
abrupt  than  usually.     (See  figs.  309  and  310.) 

When,  on  the  contrary,  the  blood-flow  into  the  ventricle 
is  abnormally  slow,  as  it  is  in  mitral  stenosis,  the  diastolic 
portion  of  the  tracing  may  be  of  much  longer  duration  than 
in  health.^     (See  fig.  311.) 

'  I  say  may  be,  for  in  mitral  stenosis  the  rhythm  is  often  perverted ;  the  left 
auricle  is  apt  to  contract  at  irregular  intervals,  and  in  some  of  the  individual 
cardiographic  curves  the  diastolic  portion  may  be  shortened,  while  in  the 
majority  it  is,  as  we  should  expect,  increased. 


Analysis  of  a  CardioorapJiic  tracing.  769 


Fig.  309. —  Cardiogram  in  a  case  of  aortic  regurgitation.  —  {After  Galabin.) 
'  The  heart  was  much  dilated,  the  apex  beat  being  in  the  sixth  intercostal  space, 
and  external  to  the  line  of  the  nipple.  The  pulse  tracing  showed  extreme 
collapse  in  the  diastolic  portion,  and  an  almost  entire  absence  of  the  tidal  wave. 
From  this  it  may  be  inferred  that  the  regurgitation  was  very  free,  and  the  contrac- 
tions of  the  heart  short  and  incomplete.  The  tracing  is  partly  inverted,  and  a 
retraction  occurs  during  the  latter  part  of  systole,  followed  by  a  sudden  recoil.' 
—(Guys  Hospita!  Reports.  1875,  p.  312.) 


Fig.  t,'^0.  — Cardiogram  froi/i  a  case  of  aortic  regurgitation  and  obstruction  com- 
bined mith  mitral  regurgitation  showing  marked  ascent  of  the  line  indicatms^ 
intra-ventricitlar pressure  during  diastole. — [After  Sansom. ) 


Fig.    311.  —  Cardiograph  ic  tracing  in  a  case  of  mitral  stenosis. — {After  Galabin. ) 
'Matilda  A.,  set.   37.     Long,  rough,  presystolic  murmur,  commencing  imme- 
diately from  the  second  sound,  and  leading  up  to  the  first  sound.      Pulse  57.' — 
{Gu/s  Hospital  Reports,  1875,  p.  314.) 

The  duration  of  the  dia.stolic  portion  of  the  tracing  in- 
dicates the  length  of  the  ventricular  diastole  ;  the  mode  of 
ascent,  the  manner  in  which  the  ventricle  is  being  filled. 

C  C  C 


/  / 


o 


Appendix. 


The  presence  of  rough  presystolic  or  diastoh'c  mitral  mur- 
murs and  thrills,  is  in  some  cases  manifested  in  the  tracing 
by  a  series  of  fine  serrated  curves,  which  occasionally  also 
mark  the  presence  of  a  rough  diastolic  aortic  murmur.^ 
(See  figs.  312  and  313.) 


Fig.  312.  Fig.  313. 

Fig.   ^12.— Cardioj^raf'/iic  tracing  in  a  case  of  mitral  stenosis. — {After  Galabin. ) 

'George  M..  ret.  19.     Long,  loud,  and  harsh  presystolic  murmur,  commencing 

immediately  from  the  second  sound  and  running  up  to  the  first  sound.      Pulse  60. 

The  letters,  indicates  the  probable  commencement  of  the  auricular  contraction.' — 

{Guys  Hospital  Reports,  1875,  p.  314.) 

Fig.  313.  —  Cardiogi-am  from  a  case  of  aortic  regurgitation.  —  [After  Galabin.) 
'  Thomas  S.,  xt.  45.     The  diastolic  murmur  was  very  loud  and  accompanied 
by  a  thrill  felt  at  the  apex.  P.  74.'—  [Guy's  Hospital  Rep07-ts,  1875,  p.  313.) 

The  exact  significance  of  the  wave  k  (see  fig.  302),  which 
occurs  near  the  commencement  of  the  diastolic  portion  of 
the  tracing  is  a  matter  of  dispute.  Dr  Galabin  thinks  that 
it  probably  indicates  a  slight  movement  forward  of  the  heart 
as  a  whole  caused  by  the  reflux  of  blood  which  closes  the 
aortic  valve.^  Dr  Sansom  has  found  the  wave  k  to  be  most 
constantl}'  associated  with  sjiddeuncss  in  the  action  of  the 
ventricles,  and  he  states  that  suddenness  of  the  action  of  the 
ventricles,  and  especially  of  the  diastolic  relaxation,  appears 
therefore  to  be  the  probable  cause  of  its  high  development.^ 

When  the  blood-flow  into  the  auricle  is  rapid,  the  wave  k 
may  not  be  perceptible,  but  may  be  merged  with  the  rapid 
rise  which  is  present  in  the  whole  of  the  diastolic  portion 
of  the  tracing.  '  In  some  cases  of  very  free  regurgitation 
with,   at    the    same    time,    gi-eat   hypertrophy,   there    is   not,' 

'  The  vibrations  of  diastolic  aortic  murmurs  are  seldom  sufficiently  rough  to  be 
demonstrated  in  this  manner. 

-   Gufs  Hospital  Reports,  1875.  p.  276. 

'  Diagnosis  of  Diseases  of  tJic  Heart,  p.  262. 


Analysis  of  a  Cardiographic  tracing.  771 

according  to  Dr  Galabin,  '  a  gradual  ascent  leading  up  to  the 
systole,  but  a  very  marked  rise  followed  by  a  fall.  It  seems 
that  the  aortic  pressure  being  raised  to  a  very  high  point  in 
systole,  causes  the  blood  to  flow  back  into  the  ventricle  with  a 
powerful  momentum  during  diastole,  which  produces  its  effect 
on  the  trace,  not  only  by  raising  the  ventricular  pressure,  but 
by  impelling  the  heart  bodily  against  the  ribs.'^  In  one  case 
of  this  description,  observed  by  Dr  Galabin,  the  impulse  cor- 
responding to  the  wave  /'  was  so  great,  as  actually  to  be  mis- 
taken for  the  apex-beat  produced  b}-  the  ventricular  contrac- 
tion itself 

The  wave  /  seems  to  correspond  to  the  blood-flow  from 
the  auricle  into  the  ventricle,  or  the  '  passive  venous  flow,'  as 
it  has  been  termed,  to  distinguish  it  from  the  blood  current  pro- 
duced by  the  contraction  of  the  muscular  wall  of  the  auricle. 

The  wave  {a')  which  is  seen  in  many  normal  tracings,  but 
only  when  the  apex-beat  is  well  defined  and  the  tracing  a 
good  one,  is  acknowledged  by  all  authorities  to  represent  the 
contraction  of  the  auricle.  When  this  wave  [a)  is  well 
marked,  we  may  infer  that  the  muscular  wall  of  the  left 
auricle  is  contracting  forcibly.  The  height  and  breadth  of 
the  wave  {a)  are  indications  of  the  force  of  the  auricular  con- 
traction, provided  that  tliere  is  no  obstruction  at  tlic  mitral 
orifice.  Its  exaggeration  is,  in  fact,  in  many  cases  an  indi- 
cation of  hypertrophy  of  the  left  auricle.  Now  hypertrophy 
of  the  left  auricle  may  occur  both  in  mitral  regurgitation  and 
in  mitral  stenosis.  In  the  former  case  (mitral  regurgitation) 
the  duration  of  the  ventricular  diastole  is  shortened,  and  the 
diastolic  portion  of  the  trace  is  represented  b}-  a  rapid  ascent  ; 
in  some  cases  of  this  description  the  wave  a  is  merged  in  the 
general  rapid  ascent,  in  others  it  is  differentiated  and  distinct. 
In  the  latter  (mitral  stenosis),  the  diastolic  portion  of  the 
tracing  is  unduly  prolonged,  and  if  the  stenosis  is  consider- 
able, even  although  the  muscular  wall  of  the  left  auricle  is 
hypertrophied,  the  wave  a  may  not  be  exaggerated,  in  fact,  it 
may  not  be  present,  the  obstruction  of  the  mitral  orifice  pre- 
venting,  as    it  were,  the   force   of  the    auricular    contraction 

'   Guy's  Hospital  Reports,  1S-5,  p.  279. 


II- 


Appendix. 


being  communicated  to  the  recording  lever  of  the  cardiograph. 
In  other  cases  of  mitral  stenosis  in  which  the  obstruction  is 
not  very  great,  and  in  which  the  wall  of  the  left  auricle  is 
hypertrophied,  the  wave  {a)  is  exaggerated.  In  others,  it  {a) 
does  not  immediately  precede  the  ventricular  systole,  but 
occurs  in  the  earlier  part  of  the  diastolic  portion  of  the  trac- 
ing, the  auricular  contraction  occurring  earlier  in  the  diastole 
than  normal.  In  exceptional  circumstances  the  rhythm  of 
the  auricular  contractions  may,  it  would  appear,  be  still 
further  interfered  with,  such  at  all  events  seems  to  be  the 
most  probable  explanation  of  a  cardiogram  published  by 
Galabin   (see   fig.    314)  ;    in    that    case,  which  was  probably, 


Fig.  314. — Cardioo}-ain  from  a  case  of  (?)  mitral  stenosis,  shoiuing  two  auricular 
contractions  {a,  a,)  for  one  ventricular  beat.— [After  Galabin. ) 


though  not  certainly,  a  case  of  mitral  stenosis,  the  diastolic 
portion  of  the  trace  was  enormously  prolonged,  and  in  man)- 
of  the  cardiographic  curves  two  auricular  contractions  ap- 
peared to  be  present  ;  in  other  words,  each  auricular  contrac- 
tion was  not,. as  under  ordinary  circumstances,  followed  by  a 
contraction  of  the  ventricle. 

The  special  characters  of  the  cardiographic  tracing  in  the 
individual  valvular  lesions  have  previous!}-  been  described, 
and  need  not  again  be  detailed. 

Inverted  tracings. — In  describing  the  manner  in  which  the 
cardiograph  is  to  be  applied,  it  has  been  stated  that  unless 
the  button  of  the  instrument  is  very  accurately  adjusted  to 
the  maximum  point  of  pulsation  of  the  apex-beat,  the  tracing 
is  apt  to  be  inverted  ;  beyond  a  certain  area  in  fact  the 
(positive)  impulse  of  the  heart  against  the  chest  wall  is 
replaced  by  (negative)  suction  or  retraction,  and  when  the 
button  of  the  cardiograph  is  placed   over  the  area  of  retrac- 


Analysis  of  a  Cardiof^raphic  tracing.  773 

tion.  a  negative  or  inverted  tracing  is  obtained.  Between  the 
(positive)  area  of  impulse  and  the  (negative)  area  of  retraction, 
there  is,  in  many  cases,  an  intermediate  area  which  yields  a 
mixed  tracing  (partly  positive  and  partly  negative.) 

Inverted  tracings  may  be  deciphered  by  means  of  a  mirror; 
or  may  be  read  as  positive  if  they  are  turned  upside  down 
and  read  from  right  to  left. 

Completely  inverted  tracings  are  of  some  value,  but  no 
importance  should  be  attached  to  mixed  tracings  (partly 
positive  and  partly  negative). 

The  following  cardiograms,  copied  from  Galabin,  are  good 
illustrations  of  negative  tracings.     (See  figs.  315,  316,  and  317.) 


FTA. 


^y  ^40 


Fig.  315. 


Fig.   ;i6. 


Fig.  317. 

Figs.  315,  316  and  317. — Itn<erted  tracin:^s.  —  {After  Galabin.) 

'  Inverted  tracings  taken  in  different  situations  from  a  healthy  heart  which 
gave  no  positive  impulse  anywhere.  Fig.  315  was  taken  near  the  usual  position 
of  the  apex  beat  ;  fig.  316  in  the  epigastrium,  to  the  left  of  the  middle  line  ;  fig. 
317,  also  in  the  epigastrium,  but  to  the  right  of  the  middle  line.' 


For  further  information  on  the  cardiograph,  the  reader  is 
referred  to  the  writings  of  Foster,^  Galabin,-  and  Sansom,^  to 
which  I  am  largely  indebted  for  much  of  my  information  on 
the  subject. 

'  A  Text  Book  of  Physiology,  l>y  Professor  A/.  Foster,  p.  138,  et  seij. 
-  On    the   Interpretation  of  Cardiographic    Tracings    by  Dr  A.   L.    Galabin 
Guy  s  Hospital  Reports,  1875,  p.  261. 

■'  Diagnosis  of  Diseases  of  the  Heart,  by  Dr  Sansoin,  p.  221. 


INDEX 


Abscess  of  the  heart,  562 

a  cause  of  aneurism  of  the  heart,  576 

of  rupture  of  the  heart,  652 

Aconite  in  the  treatment  of  pericarditis,  339 

Adherent  pericardium,  345 
diagnosis  of,  347 

physical  signs  of,  346 

prognosis  of,  352 

symptoms  of,  346 

•      treatment  of,  353 

Adventitious    products  in   the    heart — see   New- 
growths. 
Age,  in  aetiology  of  cardiac  affections,  61 
Ague-type  of  ulcerative  endocarditis,  410 
Allbutt,  Dr  Cliftbrd,  on  aetiology  of  aortic  incom- 
petence, 503 
on   morjjhia  in   mitral  dis- 
ease, 473 
Amyl  nitrite,  as  a  diuretic,  475 

in  treatment  of  angina  pectoris, 

686 
Ammonia,  in  treatment  of  cardiac  thrombi,  397 
Anaemia,  a  cause  of  fatty  heart,  639 

of  mitral  regurgitation,  425 

Ansemia,  progressive  pernicious,  treatment  of,  464 
AnBemic  murmurs,  187 

Dr  Balfour's  theory  of,  190 

purely  pulmonary,  theory  of, 

205 

•  Dr  Russell's  theory  of,  200 

Aneurism  of  the  (thoracic)  aorta,  697 

aetiology  and  pathology  of,  69S 

clinical  history  of,  701 

course  and  terminations  of,  721 

diagnosis  of,  722 

physical  signs  of,  707 

■  prognosis  of,  739 

symptoms  of,  703 

•  treatment  of,  740 

varieties  of,  697 

Aneurism  of  the  heart,  576 

etiology  of,  576 

•  diagnosis  of,  577 

pathology  of,  577 

prognosis  of,  578 

symptoms  and  physical  signs  of, 

577 

treatment  of,  579 

Aneurism  of  the  valves  of  the  heart,  404 


Angina  pectoris,  672 

Eetiology  and  pathology  of,  672 

diagnosis  of,  684 

prognosis  of,  686 

symptoms  and    physical   signs 

of,  680 

treatment  of,  688 

Aorta,  thoracic,  anatomical  course  and  relations 
of,  225 

auscultation  of,  230 

diseases  of,  690 

inspection  of,  225 

palpation  of,  228 

percussion  of,  229 

physical  examination  of,  224 

Aortic  obstruction^j^i:  Aortic  stenosis. 
Aortic  valve,  construction  of,  498,  499 

rupture  of,  501 

Aortic  incompetence,  498 

aetiology  of,  498 

clinical  history  of,  509 

diagnosis  of,  516 

pathology  of,  500 

pathological      physiology 

of,  505 . 

physical  signs  of,  51 1 

prognosis  of,  518 

symptoms  of,  509 

treatment  of,  519 

Aortic  second  sound,  accentuation  of,  145 

diminished  intensityof,  150 

Aortic  stenosis,  521 

aetiology  and  pathology  of,  521 

diagnosis  of,  526 

•  pathological  physiology  of,  522 

physical  signs  of,  524 

prognosis  of,  530 

— ■ — •  symptoms  of,  523 

treatment  of,  531 

Aortitis,  acute,  690 
Apex  of  the  heart,  bifid,  2 
Apex-beat,  loi 

•       inspection  of,  lor 

palpation  of,  103 

Apex  murmurs — see  Mitral  murmurs. 
Appendix  on  the  cardiograph,  751 
Arcus  senilis,  in  fatty  heart,  644 
Arterial -blood  supply  of  the  heart,  10 
Arterial  pycemia — see  Ulcerative  endocarditis. 


776 


Index. 


Arterial  tension,  increased,  causes  of,  58S 
Arteries  peripheral,  examination  of,  231 
Arsenic,  in  treatment  of  an?emia,  464,  47 1 
Atheroma,  691 

•       nstiology  of,  691 

diagnosis  of,  696 

pathology  of,  693 

physical  signs  of,  695 

prognosis  of,  697 

symptoms  of,  695 

treatment  nf,  697 

Atrophy  of  the  heart,  62S 

Eetiology    and     pathology 

of,  629 

diagnosis  of,  632 

•  prognosis  of,  633 

symptoms    and     physical 

signs  of,  631 

treatment  of,  633 

Atropia,  action  of,  on  the  heart,  35 
Attitude  in  cardiac  disease,  90 
Auricles,  contraction  of,  regulated  by  ventricle, 
16 

function  of,  3 

Auscultation,  134 
Auto-audible  heart  sounds,  155 
Automatic  mechanism  of  the  heart,  10,  13 


Bacteria  in   ulcerative   endocarditis — sec    Mic- 
rococci. 
Balfour,  I)r  G.  W.,  on  amvmic  murmurs,  190 

—    the  coronary  circulation, 

10 

—    the     duration    of    aortic 

aneurisms,  721 

—    iodide    of    potassium    in 

aneurism,  741,  742 

—  -    mitral  stenosis,  484,  487 

—    pulmonary  murmurs,  190 

—    reduplication     of    the 

second  sound,  166 

—    (^luincke's   pulmonary 

murmur,  554 
Barlow,  l)r,  on  the  Ktiology  of  endocarditis,  364 
— —  mitral    stenosis, 

477 

on  the  relationship  of  endocarditis 

and  chorea,  363 
Barr,  Dr,  on  reduplication  of  the  heart  sounds, 

156,  159.  164 
Bartholow,  Dr,  on  the  treatment  of  chronic  myn- 

carditis,  575 
Bazy,   M.   le  Dr,  on  the    pathology  of   angina 

pectoris,  675 
Blood-letting — sec  Venesection. 
Blood-vessels,  relationship  of,  to  the  heart,  39 

— —         tone  of,  how  regulated,  40 
Brakenridge,  Dr,  on  caffeine,  474 


Breathing,  the  condition  of,  in  cardiac  affections, 

90 
Bristowe,    Dr,   on   the  dyspnoea  of  aneurisms, 

746 
Broadbenl,    Dr,    on    the    causes    of    increased 
arterial  tension,  588 
treatment      of     endo- 
carditis, 390 

treatment  of  increased 

arterial  tension,  465 
Brunton,  Dr  Lauder,  on  angina  pectoris,  686 

casca,  471 

nitrite  of  amyl,  686 

Bulging  of  prKCordia^.f^c  Precordial  promin- 
ence. 


Caffeine,  471,  474 

Calcification  of  arteries — see  Atheroma. 

Calf,  nerves  of  the  heart  of,  1 7 

Cancer  of  the  heart,  655 

Capillary  pulse  in  aortic  incompetence,  514 

Cardiac  dulness—  sec  Dulness. 

impulse — see  Impulse. 

muscle — sec  Muscle. 

nerves,  17 

sounds — see  Sounds. 

Carditis — see  Myocarditis. 
Cardiograph,  751 

forms  of,  753 

information    to  be   derived    from, 

mode  of  application,  757 

Casca,  471 

Case-taking,  method  of,  58 

Cervical  cardiac  branches  of  the  pneumogastric, 

24  ... 

Chauveau,   Professor,   on    the   interpretation   of 
cardiographic  tracings,  762 

on     the     production    of 

murmurs,  169 
Cheyne-Stokes'  respiration,  68 

clinical  investigation  of,  So 

theories  of,  71 

Chordit  tendineiv,  rupture  of,  427 
Chorea,  endocarditis  in,  377 
Church,  Dr,  on  atrophy  of  the  heart,  630 
Circulation,  the  course  of  the,  3 

in  the  foetus,  545 

Cirrhosis  of  the  heart — see  Chronic  myocarditis. 
Cirrhosis   of  kidnev,    hvpertrophy  of  heart  in, 

588 
Cirrhosis  of  lung,  a  cause  of  dilatation  and  hyper- 
trophy of  the  heart,  598 

of  displacement  of  the 

heart,  109 
Co-arctation  of  the  aortic  arch,  746 
Cobbold,  Dr   T.  S.,  on   hydatid  disease  of  the 

heart,  656 
Colour  of  the  face  in  cardiac  affections,  87 


Index. 


Ill 


Compensation    of    cardiac    lesions,     pathology 

of'  53  ^.     . 

Complaints  of  the  patient  in  cardiac  anections, 

Concentric  hypertrophy  of  the  heart,  581 
Congenital  atrophy  of  the  heart,  629 

disease  of  the  pulmonary  artery,  542 

Convallaria  majalis,  471 
Coronary  arteries,  atheroma  of, 

circulation  in,  10 

Coronary  circulation  in  aortic  incompetence,  50S 

plexus  of  nerves,  18 

Corrigan's  pulse,  513 

Cough,  81 

Cyanosis,  87,  548 

Cyon  and  Ludwig,  Professors,  on  cardio-inhibi- 

tory  action,  29 
Cysts  in  the  heart,  656 


Deep  cardiac  plexus,  19 

Deep  cardiac  dulness — see  Dulness. 

Deep,  middle,  or  great  cardiac  nerve,  22 

Depressor  or  superior  cardiac  nerve,  30,  31,  44 

D'Espine,    Professor,    on    reduplication    of   the 

heart  sounds,  159 
Diastolic  murmurs,  174 
Dicrotic  wave  in  pulse  tracing,  251 

■  causes  of  in  health,  252 

disease,  256 

Dicrotism,  causes  of,  256 

degrees  of,  254 

Digitalis  in  mitral  cases,  470 

in  aortic  cases,  521 

Dilatation  of  the  heart,  579,  609 

jetiology  and  pathology, 

610 

diagnosis,  622 

pathological  physiology, 

617 

physical  signs,  619 

•  prognosis,  627 

symptoms,  618 

treatment,  627 

varieties,  609 

Diphtheria,  a  cause  of  ulcerative  endocarditis, 

401 
Diphtheritic  endocarditis — see  Ulcerative  endo- 
carditis. 
Displacements  of  the  heart,  105 

from  extrinsic  causes, 

107 
•         from  intrinsic  causes, 

Diuretics  in  dropsy,  475 
Dropsy,  89 

treatment  of,  475 

Drummond,    Dr    D.,    on    tracheal    nuunuir   in 

aneurism,  718 


Duchenne,  Dr,  on  faradism  in  angina  pectoris, 

688 
Dudgeon's  sphygmograph,  238 

■ advantages      claimed 

for,  235 

mode  of  applying,  246 

Dugong,  the  heart  of,  2 
Dulness,  deep  or  relative,  127 

superficial  or  absolute,  122 

Dulness,  precordial,  diminished,  132 

— —  causes  of,  133 

differential     diagnosis    of, 

Dulness,  prsecordial,  increased,  128 

differential    diagnosis    of, 

129 
Dyspnoea,  in  cardiac  affections,  66 
in  mitral  lesions,  440 


Eccentric  hypertrophy  of  the  heart,  582 
Eichhorst  on  the  action  of  the  vagus,  38 
Embolic    infarction,    a    cause    of    'accidental' 
symptoms,   65 

in    ulcerative    endocarditis, 

405 

—  in  mitral  stenosis,  483 

Endarteritis  deformans — see  Atheroma. 
Edinburgh  University  Museum,  specimens  lent 

horn.— see  figs.   17 1,  243,  244,  262,  and  28 1 
Endocardium,  diseases  of,  360 

structure  of,  366 

Endocarditis,  acute  simple,  361 

setiology  of,  361 

clinical  history  of,  368 

complications  of,  380 

diagnosis  of,  382 

onset,     course,     and 

terminations  of,  381 

pathology  and  morbid 

anatomy  of,  363 
physical  signs  of,  371 

prognosis  of,  3S4 

symptoms  of,  368 

treatment  of,  386 

varieties  of,  361 

Endocarditis,  chronic,  415 

aetiology,  415 

morbid  anatomy,  415 

results  of,  416 

Endocarditis  maligna — see  Ulcerative  E. 

ulcerative — see  Ulcerative  E. 

Endocardial  murmurs,  168 

Epigastric  pulsation,  113 

Ergotine,  in  the  treatment  of  aneurism,  743 

Eulenberg,    Professor,   on  galvanism  in   angina 

pectoris,  608 
Exocardial  murmurs,  167 
Exophthalmic  goitre,  a  cause  of  dilatation,  426 


7/8 


Index. 


Exophthalmic  goitre,  a  cause  of  mitral  incom- 
petence, 426 

palpitation, 667 

treatment  of,  464. 

Expectoration,  82 

Expression  of  the  face,  in  cardiac  afiections,  90 


Face,  colour  of,  87 
expression  of,  90 

Fagge,  Dr  Hilton,  on  fibroid  degeneration,  568 

jugular  pulsation,  536 

mitral  stenosis,  486,  4S7 

pulmonary  murmur,  554 

salicin,  392 

Fatty  degeneration  of  the  heart,  638 

aetiology  and  pathology  of,  639 

diagnosis  of,  647 

physical  signs  of,  645 

prognosis  of,  649 

symptoms  of,  644 

•    treatment  of,  650 

Fatty  infiltration  of  the  heart,  633 

aetiology  of,  633 

diagnosis  of,  637 

pathology  of,  634 

prognosis  of,  637 

symptoms  and  physical  signs  of,  636 

•    treatment  of,  638 

Family  history,  in  cardiac  afiections,  86 
Fenwick,  Dr  Bedford,  on  tricuspid  stenosis,  539 
Fibroid  degeneration — see  Chronic  myocarditis. 
Filehne,  Dr,  on  Cheyne-Stokes'  respiration,  73 
First  sound  of  the  heart — see  Sounds. 
Fleming's  sphygmograph,  235 
Flint,  Professor  A.,  on  presystolic  murmurs,  177 
Fothergill,    Dr  J.    M.,   on  hypertrophy  of  the 
heart,  592 

on  palpatation,  592 

Eraser,  Professor  T.  R.,  on  strophanthus,  471 

Fremitus,  friction,  120 

Foster,  Professor  M.,  on  cardiographic  tracings, 

760,  et  sec]. 
Friction  fremitus,  120 
Friction  sounds  in  pericarditis,  316 
Functional  affections  of  the  heart,  659 

general  pathology  of,  46 

Functional  murmurs — see  Anaemic  murmurs. 


Gairdner,  Professor,  on  the  presystolic  murmur, 
176 

on   the  diagnosis  of  fatty 

heart,  647 

on  tricuspid  stenosis,  539 

Galabin,  Dr,  on  cardiographic  tracings,  751,  et 
seq. 

on  mitral  stenotic  murmurs,  4S7 

Galabin's  cardiograph,  753 


Galvano-punctUre  in  aneurism,  743 

Gendrin,   Dr,  on  the   distinction  of  sounds  and 

murmurs,  179 
Gibson,  Dr  G. ,  on  jugular  pulse,  292 

on  the  rhythm  of  the  heart,  137 

Grave's  disease, — see  Exophthalmic  goitre. 
Great,  middle,  or  deep  cardiac  nerve,  22 
Greenfield,  Professor,  case  of  mitral   aneurism, 

403 
Gowers,  Dr,  on  acute  myocarditis,  561 
Gull,  Sir  Wm.,  on  increased  arterial  tension,  5S8 
on  the  physical  signs  of  endo- 
carditis, 379 
Guttmann,    Professor,   on   reduplication  of  first 

sound,  159 
second  sound,  166 


HaBraopericardiura,  359 

Hamilton,  Professor  D.  J.,  on   waxy  disease  of 

the  heart,  654 
Haemoptysis  in  cardiac  afiections,  82 

in  mitral  stenosis,  481-495 

Hayden,  on  reduplication  of  the  first  sound,  159 
Heart,  a  muscular  pump,  2 
a  vital  organ,  6 

abscess  of,  562 

acute  aneurism  of,  576 

aneurism  of,  576 

atrophy  of,  628 

dilatation  of,  579-609 

displacements  of,  105 

fatty  degeneration  of,  638 

fatty  infiltration  of,  633 

fibroid  disease  of,  568 

•    functional  afiections  of,  659 

general  pathology  of,  46 

hypertrophy  of,  579 

•    malposition  of,  105 

new  growths  in,  654 

pathology  of,  46 

position  of,  94 

relation  of,  to  chest  wall,  95 

rupture  of,  652 

Hesse,  Dr,  on  the  action  of  the  mitral  valve,  421 
Heubner,  Professor  von,  on  galvanism  in  angina 

pectoris,  689 
History,  the,  of  cardiac  cases,  84 

family,  86 

Hydatid  cysts,  in  the  heart,  656 
Hydropericardium,  354 

aetiology  of,  354 

diagnosis,  355 

symptoms,  355 

physical  signs,  355 

prognosis,  356 

treatment,  356 

Hydro-pneumo-pericardium,  357 


Index 


179 


Hydrops  peiricardii— .r^:^  Hydropericardium. 

Hyperdicrotism,  257 

Hyperpyrexia,  in  acute  pericarditis,  313 

treatment  of,  341 

Hypertrophy  of  tihe  heart,  579-581 

aetiology  and  pathology,  5S2 

diagnosis,  603 

prog'nosis,  606 

treatjment,  607 

Hypertrophy  of  the  left  ventricle,  586 

Ktiojlogy,  586 

consequences  of,  591 

physi^cal  signs  of,  593 

sympt.-^ms  of,  591 

Hypertrophy  of  the  left  auricle,  601 
Hypertrophy  of  the  rigL''^  auricle,  603 
Hypertrophy  of  the  right  \     'tricle,  597 
aetiology,  597       •, 

physical  signs,  6>.   ■>. 

symptoms  and  coi  icquences,  599 


Impulse  of  the  heart,  116 

celerity  of,  119 

diminished,  117 

increased,  118 

Impurity  of  the  heart  sounds,  154 

Increased intensityofcardiacsounds — sec  Sounds. 

Incompetence  of  valves,  52 

general  pathology  of,   ^2 

muscular,  51 

relative,  52 

Indurative-mediastino-pericarditis,  35  ;■ 
Infective  endocarditis — sec  Ulcerative  7.. 
Innominate  aneurisms,  737 
Inspection  of  the  prjecordia,  93 

method  of,  98 

Inspiration,  effects  of,  on  the  pulse,  261 
Intensity  of  the  cardiac  sounds — see  Sour  ds 
Intermission  of  the  pulse,  670 
Intermittent  action  of  the  heart,  670 
Intra-thoracic  tumours,  diagnosis  of,  726 
Iodide  of  potassium  in  aneurism,  741 
Iron  in  anxmia,  463 
Irregularities  of  the  pulse,  26S 

clinical  significance  of,   273 

Jaborandl,  action  of,  on  the  heart,  35 
Johnson,  Professor  G.,  on  increased  arterial  ten- 
sion, 588 

on  reduplication    of  the 

heart  sounds,  159 
Jugular  veins,  distention  of,  2S8 
— —  pulsation  in,  291 


Kussmaul,  Professor,  on  pulmonary  stenosis, 542 


J-iancereaux,    Professor,   on  the    pathology    of 

angina  pectoris,  675 
Langenbeck,  Professor,  on  ergotine  in  aneurism, 

743 
Legg,  Dr  Wickham,  on  cardiac  aneurisms,  576 
Loudness   or   intensity   of  cardiac  sounds — see 

Sounds 
Louis,  Professor,  on  atrophy  of  the  heart,  630 
Lower  cardiac  nerve,  22 
Ludwig  on  the  action  of  the  mitral  valve,  421 

on  cardiac  inhibitory  action,  29 


Macalister,  Dr  D.,  on  the  action  of  the  mitral 

valve,  421 
Maclagan,  Dr,  on  salicin,  389 
Mahomed's  sphygmograph,  236 
.Marey,  M.,  on  cardiographic  tracings,  762 

cardiograph,   756 

1  sphygmograph,  236 

'  Martin,  Professor,  on  the  coronary  circulation, 
10 
Micrococci  in  simple  endocarditis,  399 

in  ulcerative  endocarditis,  398,  399 

Middle,  deep,  or  great  cardiac  nerve,  22 

Milk  spots,  structure  of,  302 

Mitral  first  sound,  increased  intensity  of,  147 

diminished  intensity  of,  151 

Mitral  incompetence,  421 

aHiology  and  pathology  of,  42 1 

clinical  history  of,  437 

diagnosis  of,  448 

•  pathological  physiologyof,42S 

physical  signs  of,  441 

prognosis  of,  445 

treatment  of,  462 

varieties  of,  425 

Mitral  regurgitation — see  Mitral  incompetence 
Mitral  stenosis,  477 

aetiology  of,  477 

clinical  history  of,  483 

diagnosis  of,  493 

•  pathology  of,  478 

pathological  physiology  of,  479 

physical  signs  of,  484 

prognosis  of,  496 

symptoms  of,  483 

■ treatment  of,  497 

Mitral  valve,  construction  and  action  of,  421 

Monocrotic  pulse,  258 

Morphia  in  mitral  disease,  473 

Moxon  and  Wilks,    Drs,   on  the  production  of 

vegetations,  365 
Muffling  of  the  heart  sounds,  154 
Murmurs,  167 

—  auKmic,  187 

—  clinical  investigation  of,   172 

—  combinations  of,  178 


jSo 


Index. 


Murmurs,  differential  diagnosis  of,  208 

—  diastolic,  174 

—  direction  of  propagation  of,  1S2 

—  endocardial,  168 

—  exocardial,  167 

—  friction,   168 
functional,  187 
organic,  171 

—  pericardial,  316 

—  pericardial-pleural  friction,  168 

—  points  of  maximum  intensity  of,  iSo 

—  post-diastolic,  178 

—  presystolic,  176,  485 

—  rhythm  of,  172 

—  sound  characters  of,  186 

—  systolic,  172 

—  venous,  170 

Murray,  Dr  Wm.,  his  case  of  neurotic  palpita- 
tion of  the  aorta,  724 
Murrell,    Dr,  on  nitro-glycerine  in  angina  pec- 
toris, 687 
Muscarin,  action  of,  on  the  heart,  35 
Muscle,  cardiac,  how  stimulated,  1 1 

rhythmical  properties  of,  11,  14 

structure  and  characters  of,  7, 14 

Muscular  incompetence,  51,  425 
Myocardium,  diseases  of,  560 
Myocarditis,  acute,  560 

aetiology  of,  561 

diagnosis  of,  564 

pathology  of,  561 

physical  signs  of,  564 

• prognosis  of,  566 

symptoms  of,  564 

treatment  of,  566 

Myocarditis,  chronic,  568 

Ktiology  of,  568 

•  diagnosis  of,  574 

pathology  of,  571 

physical  signs  of,  573 

prognosis  of,  574 

-  —  symptoms  of,  573 
treatment  of,  575 

Myotatic  theory  of  cardiac  contractions,   11,   14 


^aunyn,  Professor,  on  the  pulmonary  murmur 

190 
Neuroses  of  the  heart,  659 
Nervous  supply  of  the  heart,  17 

(sensory),  673 

New  growths  in  the  heart,  654 

Ktiology  and  pathology  of,  654 

diagnosis  of,  657 

prognosis  of,  658 

symptoms  and  physical  signs  of,  657 

treatment  of,  658 

Nitrite  of  amyl  in  angina  pectoris,  686 


Nitro-glycerine  in  angina  pectoris,  fS7 
Nutrition,  the  state  of,  in  cardiac  .'  ffections,  91 


Occupation,  influence  of,  ir  the  production  of 

cardiac  disease,  62 
Ogle,  Dr,  on  blood -cysts  in  t  le  heart,  656 
Organic  affections  of  the  heait, 

general  pa  hology  of,  48 

Orthopncea,  68 

Osier,    Professor,    on    ulceraave    endocarditis, 

397-  399 


Pain,  cardiac,  67^   .  ■ 

Pallor  of  the  fac  'i  cardiac  cases,  89 

Palpation,  102   - 

Palpitation,  65' 

retiology  and  pathology  of,  659 

di..gnosis  of,  664 

prognosis  of,  668 

■ s^  mptoms  and  physical  signs  of,  662 

t  eatment  of,  668 

Paracentesis  pericardii,  343 
Partial  aneur.sms  of  the  heart — see  Aneurisms 
Peacock,  Dr,  on  pulmonary  stenosis,  544 
Percussion,  121 

stroke   of  sphygmographic   tracing, 

248 

wave,  250 

Pericardii    adhesions,  345 

effusion,  319 

fremitus,  121 

friction,  316 

pleural-friction,    327 

Pericajdium,  diseases  of,  296 

structure  of,  303 

Perica'ditis,  acute,  297 

setiology  of,  298 

clinical  history  of,  306 

diagnosis  of,  325 

differential  diagnosis  of,  327 

onset,  course  and  terminations  of, 

325 

pathology  and  morbid  anatomy  of, 

300 

physical  signs  of,  314 

prognosis  of,  334 

symptoms  of,  307,  322 

treatment  of,  336 

varieties  of,  297 

Pericarditis,  chronic,  353 

aetiology  and  pathology  of,  353 

diagnosis  of,  354 

physical  signs  of,  354 

prognosis  of,  354 

symptoms  of,  353 

treatment  of,  354 


Index. 


/' 


I 


Peter,    Professor,   on   the  pathology  of  angina 
pectoris,  675 

un     venesection     in     angina 

pectoris,  687 
Pettigrew,  Professor,  on  the  cardiac  nerves,  17 
Physical  examination  of  the  heart,  92 

of    the    aorta    and    great 

vessels,  224 

of  the  veins,  287 

Physiognomy,  the,  of  cardiac  cases,  86 
Pleuritic  friction,  121 

pain  in  pericarditis,  310,  312 

Pneumogastric,  its  cardiac  branches,  24 

its  action  on  the  heart,  28,  34 

its  inhibitory  action,  28,  31 

its  trophic  function,  33 

Pneumonia  in  ulcerative  endocarditis,  406 
Pneumo-pericardium,  357 

Prsecordia,  boundaries  of,  95 

condition  of  skin  of,  102 

flattening  of,  100 

inspection  of,  93 

prominence  of,  98 

Prtecordial  dulness — see  Dulness. 

Prsecordial  thrills — see  Thrills. 

Predicrotic  wave  of  sphygmographic  tracing,  25S 

absence  of,  259 

Present  condition  of  the  patient,  86 
Presystolic  murmurs,  176,485 
Pseudo-angina  pectoris,  672,  680 
Pulmonary  murmurs  of  anasmia,  190 
Pulmonary  incompetence,  557 

letiology  of,  557  .   . 

Pulmonary  incompetence,  clinical  history  of,  558 

diagnosis  of,  559 

pathological  physiology  of,  557 

physical  signs  of,  55S 

prognosis  of,  559 

treatment  of,  559 

Pulmonary  second  sound,  accentuation  of,   146 

diminished  intensity  of,  151 

Pulmonary  stenosis,  541 

•  cetiology  of,  541 

clinical  history  of,  54S 

• diagnosis  of,  552 

difterential  diagnosis  of,  555 

pathology  of,  542 

pathological  physiology  of, 

544 

physical  signs  of,  550 

• prognosis  of,  556  i 

symptoms  of,  548 

treatment  of,  557 

Pulse,  condition  of  arterial  coats,  282 

dicrotic,  256 

effects  of  respiration  on,  271 

examination  of,  233 

frequency  of,  263 

hyperdicrotic,  257 


Pulse,  inequalities  in  two  wrists,  268 

in  aneurism,  2S3,  715 

in  aortic  incompetence,  513 

stenosis,  525 

■ in  mitral  incompetence,  443 

stenosis,  482,  493 

irregularities  of,  268 

inspection  of,  234 

large,  275 

palpation  of,  233 

quick,  264 

rhythm  of,  268 

slow,  266 

small,  276 

sphygmographic  characters  of,  271,  280 

strength  of,  278 

• tension  of,  278 

variability  of,  267 

■  volume  of,  275 

weak,  278 

Pulsus,  bigeminus,  270 

paradoxicus,  272 

trigeminus,  270 

Pysemic  type  of  ulcerative  endocarditis,  409 


Quincke,  Professor,  on  pulmonary  murmurs,  553 


Reduplication  of  the  heart  sounds,  156 

• • first  sound,  157 

second  sound,  162 

Reflex  theory  of  cardiac  contractions,  12 
Regions  on  the  front  of  the  chest,  95 
Relative  cardiac  dulness — see  Dulness. 
Relative  incompetence  of  aortic  valve,  505 

of  mitral  valve,  52,  426 

of  tricuspid  valve,  532 

Respiratory    line    of    sphygmographic   tracing, 

261 
Respiration,  effect  on  pulse,  261 
Rest  in  treatment  of  aneurism,  740 

endocarditis,  387 

Rheumatism,  acute,   method  of  case-taking  in, 

392 
Rhythm  of  cardiac  contractions,  1 19 
Rhythmical  movements  of  heart,  causes  of,  1 1 
Richardson,  Dr  B.  W.,  on  treatment  of  cardiac 

thrombi,  397 
Ringer,  Professor  .Sydney,  on  treatment  of  peri- 
carditis, 339,341 
on    the    administra- 
tion of  digitalis,  470 
Rosenstein,  Professor,  on  the  aetiology  of  simple 
endocarditis,  363 
on  the  jetiology  of  ulcera- 
tive endocarditis,  398 


782 


Index. 


Rupture  of  tlie  heart,  652 

Ktiology    and     pathology 

of,  652 

diagnosis  of,  654 

prognosis  of,  654 

symptoms    and     physical 

signs  of,  653 

treatment  of,  654 

Russell,    Dr,    on    the    pulmonary    murmur    of 
anaemia,  200 

—  the  position  of  the  appendix  of 

left  auricle  in  ana;mia,  196 
Rutherford,      Professor,     on     cardio-inhibitory 
action,  29 


Salicin  and  its  compounds  in  endocarditis,  38S 
in  pericarditis,   337 

Sansom,  Dr,  on  Cheyne-Stokes'  respiration,  72 

the  Ktiolog)'  of  endocarditis,  361 

mitral    stenosis, 

477 

cardiographic  tracings,   751    et 

set], 

nutrient  enemata,  476 

presystolic  murmurs,  485,  494 

— —  reduplication    of    first    sound, 

• ■  reduplication  of  second  sound, 

165 

■  treatment      of      exophthalmic 

goitre,  465 

Saundby,  Dr,  on  increased  arterial  tension,  589 

Septic  endocarditis— j-^^  Ulcerative  endocarditis. 

Sewall    and    Donaldson,   Drs,   on    intra-cardiac 

blood-pressure,  12 

on  the  rhythmical 

movements  of  heart,  13 
Sex,  influence  of,  in  cardiac  affections,  62 
Sibson,  Dr,  on  the  setiology  of  endocarditis,  362 

—  delirium  in  pericarditis,  313 

— pain  in  pericarditis,  310 

—  the   position  of  the   pulmonary 

artery,  191 

—  the  pathology- of  endocarditis,  364 

—  the  physical  signs  of  endocarditis, 

377 
—  the  prevention  of  endocarditis, 

387 

—  thesymptoms  of  endocarditis,  368 

—  the  relationship  of  the  heart  to 

the  front  wall  of  the  chest,  96 
—  the  position  of  the  cardiac  valves, 

139   .  . 

. — the   position    of  the    pulmonary 

artery,  191 
Sinus  venosus,  activity  of  its  ganglia,  13 
Sounds  of  the  heart,  absolute  modifications  of 
(murmurs),    167 


Sounds  of  the  heart,  alterationsof,  indisease,  141 

aortic  second,  145,  150 

auto-audible,  155 

causes  of,  135 

duration  of,  153 

impurity  of,  1=14 

individual,  13S 

intensity  of,  increased,   143 

diminished  149 

mitral  first,  147,  151 

metallic  character  of,  155 

■  mode  of  distinguishing,  141 

muffling  of,  154 

reduplications  of,  156 

points  of  maximum  inten- 
sity of,  138 

position  of,  in  disease.  166 

pulmonary  second,  146, 151 

tone  of,  154 

tricuspid  first,  147,  153 

Sphygmograph    235 

application  of,  240 

diagnostic  value  of,  234 

Dudgeon's,  258 

Fleming's,  235 

forms  of,  235 

Marey's,  236 

Mahomed's,  236 

Sphygmographic  tracing,  analysis  of,  247 

best,    how    obtained, 

244 

good,    characters     of, 

242 

normal,  248 

in     aortic      incompe- 
tence, 513 

■    stenosis,  525 

in      mitral      incompe- 
tence, 444 

in  mitral  stenosis,  493 

Spontaneous  rupture  of  the  heart,  652 

Stimulants  in  mitral  disease,  472 

Stokes,   Dr,   on   systolic   murmur  in   aneurism. 

Stenosis  of  valves,  general  pathology  of,  52 

Strophanthus,  471 

Sturges,  Dr,  on  endocarditis  in  chorea,  377 

pericarditis,  337 

Sturge,   Dr  A.,  on  the  pathology  of  angina  pec- 
toris, 677 
Subcutaneous  dropsy — see  Dropsy. 
.Superficial  cardiac  dulness — see  Dulness. 
-Sutton  Dr,  on  increased  arterial  tension,  588 
on  the  physical  signs  of  endocarditis 

377 
Superior  cardiac,  or  depressor  nerve,  29 
.Superficial  cardiac  plexus,  19 
Superficial  or  upper  cardiac  nerve,  21 
Sympathetic  nerve,  its  cardiac  branches,  21 


Index. 


78. 


Sympathetic  nerve,  its  action  on  the  heart,  38 
Symptoms  in  cardiac  cases,  61 

accidental,  65 

causes  of,  64 

classes  of,  63 

comparative    value    of   symptoms 

and  signs,  83 

—  —         mechanical,  64 

pressure,  66 

subjective,  62 

summary  of,  61 

Syphilis,  a  cause  of  frequent  aneurism,  699 

ulcerative  endocar- 
ditis, 402 
Systolic  murmurs — see  Murmurs. 

Tension  of  the  pulse —  sec  Pulse. 

Tidal  wave — see  Predicrotic  wave. 

Thoracic  cardiac  branches  of  the  vagus,  24 

Thrills,  praecordial,  120 

Thrombi  in  the  heart,  397 

Tortoise,  Ur  Gaskell's  observations  on  the  heart 

of,  II 
Traube,    Professor,  on  Cheyne  Stokes'   respira- 
tion, 71 

on  increased  arterial  tension,  588 

Tricuspid  first  sound,  accentuation  of,  147 

diminished  intensity  of,  153 

Tricuspid  incompetence,  531 

aetiology  and  pathology 

of,  531 

clinical  history  of,  534 

diagnosis  of,  537 

pathological  physiology 

of,  533 . 

physical  signs  of,  535 

prognosis  of,  538 

symptoms  of,  534 

treatment  of,  539 

Tricuspid  stenosis,  539 

.Tjtiology  of,  539 

diagnosis  of,  541 

pathological  physiology  of,  540 

physical  signs  of,  541 

symptoms  of,  540 

treatment,  541 

Trophic  function  of  the  vagus — jafPneumogastric. 
Typhoid  type  of  ulcerative  endocarditis,  408 
Tubercle  in  the  heart,  655 
Tufnell  Mr,  on  the  treatment  of  aneurism,  741 
Tumours  of  the  heart — see  New  growths,. 
Turner,  Professor,  specimens  lent  by — see  figs. 

171,  242,  244,  262,  281 
Turner,    Dr  Charlewood,   on  fibroid   degenera- 
tion, 572 

Ulcerative  endocarditis,  397 
aetiology  of,  398 


Ulcerative  Endocarditis,  clinical  history  of,  406 

complications  of,  405 

definition  of,  398 

diagnosis  of,  410 

differential  diagnosis  of, 

411 

duration  of,  410 

onset  of,  406 

pathology  of,  402 

physical  signs  of,  407 

prognosis  of,  414 

symptoms  of,  407 

termination  of,  410 

treatment  of,  414 

types  of,  407 

Upper  or  superficial  cardiac  nerve,  21 

Urari,  its  action  on  the  heart,  35 

Vagus— jf^  Pneumogastric 
Valvular  lesions,  chronic,  416 

aetiology  of,  416 

pathological  physiology  of,  418 

\'arnish  for  sphygniograph,  242 
V'aso-motor  centre,  41 
Vaso-dilator  nerves,  43 
Veins,  auscultation  of,  294 

—  distention  of,  2S8 

—  examination  of,  287 

—  inspection  of  288 

—  jugular — see  Jugular  veins 

—  palpation  of,  294 

—  pulsation  in,  293,  514 
V^enesection  in  mitral  disease,  474 
Venous  congestion,  treatment  of,  472 
\'enous  murniurs,  294 

Venous  hum,  170,  294 

Venous  pulse  in  aortic  incompetence,  514 

Ventricle,  function  of,  3 

^ATalshe,  Dr,  on  acute  aortitis,  691 

on  coarctation  of  the  aorta,  748 

on  murmurs,  188 

on  the  position  of  the  innomin- 
ate artery,  738 

on  the  position  of  the  heart  with 

regard  to  the  front  wall  of  the 
chest,  96 

on  the  position  of  the  valves  of 

the  heart,  139 
Watteville,  Dr  de,  on  galvano  puncture,  744 
Waxy  degeneration  of  the  heart,  654 
Wilks    and    Moxon,    Drs,    on  the    mechanica. 
production  of  vegetations,  365 
Wyllie,  Dr,  case  of  blood  cyst,  656 

on  the  dyspnoea  of  chronic  Bright's 

disease,  71 

Zander,  Dr,  on  the  trophic  action  of  the  vagus,  38 


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UNIVERSITY  OF  CALIFORNIA  LIBRARY 

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